Neuroscience reagents: Novus Biologicals

NB100-1028

AIF-1/Iba1 Antibody

(21 Reviews)

(520 Publications)

0.1 mg

NB100-1028

GM1 effects on brain microglia in vivo, after peripheral administration of LPS. Immunoblot in whole brain lysates and densitometric analysis show LPS-dependent increase in AIF-1/Iba1 expression. Image collected and cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/34991625/) licensed under a CC-BY license.

Reactive microglia (green) in peritumoral area of IC injected human glioblastoma cells in mouse brain. NeuN (red), DAPI (blue). Antibody at 1:250. IHC image submitted by a verified customer review.

AIF-1/Iba1 in canine brain. Primary antibody used at 1 ug/mL and incubated with tissue for 30 minutes at room temperature. IHC-P image submitted by a verified customer review.

Staining in mouse brain using AIF-1/Iba1 Antibody. IHC-P image submitted by a verified customer review.

Brown arrow= AIF-1/Iba1 positive cells, Green arrow= mTOR positive cells, Black arrow= mTOR and AIF-1/Iba1 positive cells. IHC-P image submitted by a verified customer review.

Staining in rat hippocampus using AIF-1/Iba1 Antibody. IHC-Fr image submitted by a verified customer review.

Feline optic nerve microglia were immunolabeled with AIF-1/Iba1 Antibody (green), DAPI (blue). Imaging was performed using an epifluorescence microscope. IHC-Fr image submitted by a verified customer review.

Mouse dorsal root ganglia. AIF-1/Iba1 expression in reactive macrophages. Maximum intensity z-projection from 3D images. IHC image submitted by a verified customer review.

Staining in mouse brain using AIF-1/Iba1 Antibody. IHC image submitted by a verified customer review.

Analysis of LPS injected mouse brain tissue, 20 um thickness, frozen. Primary antibody dilution, 1:200. Secondary antibody CY3. Mounted with DAPI mount. Image from verified customer review.

AIF-1/Iba1 staining of AD mouse model (hippocampus). Image from verified customer review.

Negative Control showing staining of paraffin embedded Human Spleen, with no primary antibody.

(0.1ug/ml) staining of Mouse Lymph node lysate (35ug protein in RIPA buffer). Detected by chemiluminescence.

(1ug/ml) staining of Human Frontal Cortex (A) and (0.1ug/ml) Mouse (B) and Rat (C) Brain lysate (35ug protein in RIPA buffer). Detected by chemiluminescence.

(8ug/ml) staining of paraffin embedded Human Spleen. Heat induced antigen retrieval with citrate buffer Ph 6, HRP-staining.

Immunohistochemistry-Paraffin: Goat Polyclonal AIF-1/Iba1 Antibody [NB100-1028] - AIF-1/Iba1 immunoreactivity in an FFPE section of mouse spleen. NB100-1028 was diluted to 1ug per mL and was left on tissue sections for 30m at room temperature. Secondary was horse anti goat HRP polymer. Image from a verified customer review.

Immunohistochemistry-Paraffin: Goat Polyclonal AIF-1/Iba1 Antibody [NB100-1028] - AIF-1/Iba1 immunoreactivity in an FFPE section of human tonsil. NB100-1028 was diluted to 1ug per mL and was left on tissue sections for 30m at room temperature. Secondary was horse anti goat HRP polymer. Image from a verified customer review.

Immunohistochemistry-Paraffin: Goat Polyclonal AIF-1/Iba1 Antibody [NB100-1028] - AIF-1/Iba1 immunoreactivity in an FFPE section of equine spleen. NB100-1028 was diluted to 1ug per mL and was left on tissue sections for 30m at room temperature. Secondary was equine anti goat HRP polymer. Image from a verified customer review.

Immunocytochemistry/ Immunofluorescence: AIF-1/Iba1 Antibody [NB100-1028] - Microglia proliferate in non‐APP mice upon peripheral immune challengeA, BIba‐1, Ki67, & DAPI staining in the cortex & hippocampus of wild‐type & Nlrp3−/− (5 & 15 months old). Microglia proliferate upon LPS injection (white arrows). Non‐microglia cells proliferation was observed as well (yellow arrows). Scale bar: 20 μm.CQuantification of microglial proliferation in cortex (left panel) & hippocampus (right panel) (mean of 5 ± SEM; two‐way ANOVA followed by Tukey's post hoc test, *P 1.5, FDR-corrected p1.5, FDR-corrected p<0.05) to identify GO terms, including inflammatory response (b). The volcano plot shows significant DEGs derived from the NanoString analysis of the brains of Plcg2 inactivation (PLCG2 inact, n=3) & WT (n=3) mice (1-month male) (c). Immunostaining of microglial markers with IBA1 (green) & P2RY12 (red) & quantification of percent area in brain sections of 1-month-old male WT & PLCG2 inact demonstrate unchanged microglial morphology & area coverage (d). GO gene ontology, BP biological process, DEGs differentially expressed genes, FDR false discovery rate Image collected & cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/35180881), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Immunocytochemistry/ Immunofluorescence: AIF-1/Iba1 Antibody [NB100-1028] - Representative & quantitative immunohistochemistry of the peri-infarct cortex before the bregma (coordinate + 0.58) in normal WT, normal sEH KO, MCAO WT, MCAO sEH KO, MCAO with vehicle treatment & MCAO with AUDA treatment mice (n = 2 for normal groups, n = 5–6 for all groups subjected to MCAO). (A–F, S) The number of CD31-positive endothelial cells significantly increased in the sEH KO before & after MCAO & post-MCAO AUDA-treated mice, while (G–L) Note the increased phosphorylated TrkB (p-TrkB) immunoreactivity that partially co-localized with NeuN-positive neurons, particularly in the sEH KO & AUDA-treated mice (arrows) (T). The percentage of NeuN- & p-TrkB-positive double labeling in the neuronal population was significantly increased compared to that in the corresponding controls. (M–R, U–V) GFAP-positive astrogliosis & Iba1-positive microglial infiltration decreased in post-MCAO sEH KO & AUDA treatment groups relative to that in the corresponding controls. The scale bar represents 50 µm. *p < 0.05, **p < 0.01, ***p < 0.001. Image collected & cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/29311641), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Immunocytochemistry/ Immunofluorescence: AIF-1/Iba1 Antibody [NB100-1028] - Norgestrel reduces pro-inflammatory & promotes anti-inflammatory phenotypes in rd10 microglia.(A) RT-qPCR analysis detected similar levels of mRNAs encoding progesterone receptor membrane complexes 1 & 2 (PGRMC1, PGRMC2) & all three membrane progesterone receptor isoforms, alpha , beta & gamma (mPR alpha , mPR beta , mPR gamma ) in rd10 retinal microglial cells. Classical progesterone receptor (PR A/B) was not expressed. Actin, HPRT & GAPDH served as reference genes. (B) Immunolabeling confirmed the presence of these progesterone receptors in primary rd10 microglial cells. Hoechst (blue) staining reveals the cell nuclei. Scale bar represents 10μm. (C) Fluorescent microscopic images of primary rd10 microglia immunolabeled for (C) (i) markers of activation (CD68) & pro-inflammation (M1) (iNOS) & (C) (ii) anti-inflammatory activation (M2) (MRC1); after treatment with 20 μM Norgestrel over 24h. Norgestrel reduced pro-inflammatory & increased anti-inflammatory markers in rd10 microglia. Scale bar 10μm. (D) Quantification of fluorescence intensity of (D) (i) CD68 & iNOS & (D) (ii) MRC1 in primary rd10 microglial cultures following Norgestrel treatment over 24h. N = 8 mice, n = 4 technical replicates per group. (E) Nitrite concentration in the media of rd10 microglia in vitro treated with Norgestrel or vehicle over 24hr. Norgestrel significantly reduced nitrite release from rd10 microglia. N = 8 biological replicates, n = 2 technical replicates per sample. Results are presented as mean ± SEM (t-test, *p<0.05, ***p<0.005, ****p<0.001). Image collected & cropped by CiteAb from the following publication (//dx.plos.org/10.1371/journal.pone.0165197), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Immunohistochemistry: AIF-1/Iba1 Antibody [NB100-1028] - Temporal activation of caspase-8 in Iba1-positive myeloid cells. Frozen tissue sections from mice upon pMCAO (n = 9) were analyzed by immunohistochemistry for expression of active caspase-8 or for expression of the microglia/macrophage marker Iba1. The contralateral side to the ischemic area was used an internal control for each animal. A small increase in body size of Iba1 positive cells was detected in the peri-infarct area at 6 h, with larger increase in cell body & numbers of cells expressing Iba1 detected at 24 & 48 h post occlusion (a). Cleaved caspase-8 was detected at low levels at 6 h, but a significant increase in expression levels was observed at 24 & 48 h in the peri-infarct area, but not at the contralateral side (a). Double immunofluorescent staining revealed that increased active caspase-8 expression was localized in Iba1-positive cells (b). Scale bar represent 100 μm in IHC images (a) & 10 μm in IF images (b) Image collected & cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/27566702), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Western Blot: AIF-1/Iba1 Antibody [NB100-1028] - GM1 effects on brain microglia in vivo, after peripheral administration of LPS. A Schematic representation of in vivo administration of GM1 after LPS-induced systemic inflammation in mice (N = 5 per treatment). B Representative images of Iba-1 stained microglia in the cortex of control animals infused with vehicle (CTRL) or GM1 (CTRL + GM1), & in animals treated with LPS & subsequently infused with vehicle artificial cerebrospinal fluid (LPS) or GM1 (LPS + GM1). C Immunoblot in whole brain lysates & densitometric analysis show LPS-dependent increase in Iba 1 expression. D Cortical & striatal microglia (Iba-1+ cells) cell body area quantified with MetaXpress software. GM1 administration significantly decreases cell body area in the cortex, but not in the striatum. E IL-6 protein levels in whole mouse brain homogenate. aCSF, artificial cerebrospinal fluid. Bars show mean values ± STDEV. Two-way ANOVA with Tukey’s multiple comparisons test; *p < 0.05, **p < 0.01, ***p < 0.001 Image collected & cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/34991625), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Immunocytochemistry/ Immunofluorescence: AIF-1/Iba1 Antibody [NB100-1028] - ABIN1 knockdown increases proinflammatory cytokine production & microglial activation. (a-b) Levels of the ABIN1 mRNA & protein were detected 24 h after reperfusion using RT-qPCR & western blot, respectively, to confirm the efficiency of ABIN1 gene knockdown (n = 5 rats per group). (c) ELISA was used to detect the concentrations of TNF-alpha , IL-1 beta & MCP-1 in the peri-infarct cortex at 24 h after reperfusion (n = 5 rats per group). (d) Microglial morphology was observed using immunofluorescence staining for Iba-1 (green) in the peri-infarct cortex at 24 h after reperfusion (n = 3 rats per group). Scale bar = 50 μm. (e & f) Quantification of microglia process endpoints & cell & process lengths/cell (∗∗P < 0.01 compared to the sham group; ##P < 0.01 compared to the MCAO/R group). Image collected & cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/33110436), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Immunocytochemistry/ Immunofluorescence: AIF-1/Iba1 Antibody [NB100-1028] - SCF+G-CSF treatment increases TREM2 expression in the Iba1+ microglia/macrophages surrounding the 6E10+ senile plaques. (A) Representative confocal images of TREM2 (red), 6E10 (purple) & Iba1 (green) triple immunofluorescence staining in the brains of aged APP/PS1 mice. Blue: Nuclear counterstaining by DAPI. (B) Representative orthographic view of z-stack images (12 z-stacks with 1μm intervals) illustrates the location & interaction of TREM2 + cells (red) & 6E10+ A beta plaques (white) in the brains of aged APP/PS1 mice. (C) Quantification data show the percentage of TREM2+ area surrounding the 6E10+ A beta plaques (within 10μm from the border of the A beta plaques) in the brains of aged APP/PS1 mice with or without SCF+G-CSF treatment. (D) Representative orthographic view of z-stack images (12 z-stacks with 1μm intervals) displays the location & interaction of TREM2+/Iba1+ co-expressing cells (yellow) & 6E10+ A beta plaques (white) in the brains of APP/PS1 mice. (E) Quantification data show the percentage of TREM2+/Iba1+ co-expression area in the total of Iba1+ area in the vicinity of 6E10+ A beta plaques in the brains of aged APP/PS1 mice with or without SCF+G-CSF treatment. N=4-5. Mean ± SEM. * p<0.05 by Student’s t-test. Image collected & cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/33269098), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Immunocytochemistry/ Immunofluorescence: AIF-1/Iba1 Antibody [NB100-1028] - SCF+G-CSF treatment increases the association of Iba1+ microglia/macrophages with senile plaques & enhances uptake of 4G8+ A beta by the Iba1+ microglia/macrophages in the brains of aged APP/PS1 mice. (A) Representative confocal images illustrate the association of Iba1+ cells (green) with 4G8+ A beta plaques (red) in the brains of aged APP/PS1 mice. Blue: Nuclear counterstaining by DAPI. (B) Quantification of the percentage of Iba1+ area in/surrounding the 4G8+ A beta plaques in the brains of aged APP/PS1 mice with or without SCF+G-CSF treatment. (C) Representative 3-dimensional projected images reveal the overlapped (yellow) Iba1+ cells (green) with 4G8+ A beta (red) in the brains of aged APP/PS1 mice. The white arrows indicate the co-expression (yellow) of 4G8+ A beta & Iba1+ cells in the brains of aged APP/PS1 mice. (D & E) Representative orthographic view of z-stack images (12 z-stacks with 1μm intervals) shows the co-expression (yellow) of 4G8+ A beta (red) & Iba1+ cells (green) in the brains of aged APP/PS1 mice. (F) Quantification data present the percentage of 4G8+ A beta volume within the Iba1+ cells in the brains of aged APP/PS1 mice treated with or without SCF+G-CSF. N=4-5. Mean ± SEM. *p<0.05 by Student’s t-test. Image collected & cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/33269098), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Immunocytochemistry/ Immunofluorescence: AIF-1/Iba1 Antibody [NB100-1028] - Antibody-mediated Nogo-A blockade decreases the number of cells expressing TNF alpha without affecting the number of Iba1-positive monocytes.Cells expressing TNF alpha , Iba1, & CD68 were labeled on cryosections by immunofluorescence in 4 mouse retinae, 24 h after control IgG or 11C7 injection. a Retinal sections showed many TNF alpha -containing cells located in the inner retina, between the outer plexiform layer & the ganglion cell layer 1 day after control IgG injection. A majority of cells was positive for Iba1 & exhibited vesicular staining of the lysosomal protein CD68, indicating their active state. b The injection of 11C7 strongly attenuated TNF alpha & CD68 expression & to a lower extent the intensity of Iba1 in macrophages/microglia. c Quantification of the number of cells expressing TNF alpha & Iba1 suggesting potent & specific effects of 11C7 on TNF alpha cytokine reduction. Six sections were examined for each retina. Statistics: one-way ANOVA, Dunnett’s post hoc test, **P < 0.01; ****P < 0.0001. Scale bars = 50 μm. Image collected & cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/32029703), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Immunocytochemistry/ Immunofluorescence: AIF-1/Iba1 Antibody [NB100-1028] - The presence or absence of TRPV1 influences microglial pathophysiological changes in recurrent febrile seizures mice. (A) Images of the cortex immunostained for the microglial marker Iba-1 (visualized in green FITC) & the lysosomal marker CD68/ED1 (visualized in red Alexa Fluor 594) & DAPI (visualized in blue) 5 days after rFS from wild type (WT) & TRPV1−/− mice (Scale bars: 50 μm). (B,C) Bar graph of quantification of Iba1+(B) & Iba1+ ED1+(C) in 5 days after rFS mice cortex. (D) Representative photomicrographs of different microglial morphological subtypes including resting/ramified (Ram), hypertrophic/intermediate (Inter) & round/ameboid (Amoeboid; Scale bars: 5 μm). (E) Quantification of relative percentage of microglia with different morphologies in the cortex of WT & TRPV1−/− mice (n = 6 per groups, **p < 0.01, ***p < 0.001, two-way ANOVA followed by Tukey’s multiple comparisons). (F–H) Representative Immunoblot bands (F) & densitometric analysis of Iba1 expression (G) & ED1 expression (H) were significantly increased in rFS from WT mice than in TRPV1−/− mice. Data were presented as means ± SEM, n = 6 per groups, *p < 0.05, **p < 0.01, ***p < 0.001, two-way ANOVA followed by Tukey’s multiple comparisons. Image collected & cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/31680864), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Immunohistochemistry-Frozen: Goat Polyclonal AIF-1/Iba1 Antibody [NB100-1028] - AD Mouse Model. FxFr:10 µm thickness 1:200. Secondary antibody AF647. Image from a verified customer review.

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Reactivity: Hu, Mu, Rt, Ca, Eq, Fe, Po

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NB400-105

ABCA1 Antibody - BSA Free

(7 Reviews)

(419 Publications)

0.1 ml

NB400-105

Formalin-fixed paraffin-embedded tissue sections of human prostate cancer were probed for ABCA1 mRNA (ACD RNAScope Probe, catalog # 432291; Fast Red chromogen, ACD catalog # 322360). Adjacent tissue section was processed for immunohistochemistry using rabbit polyclonal (Novus Biologicals catalog # NB400-105) at 1.5ug/mL with overnight incubation at 4 degrees Celsius followed by incubation with anti-rabbit IgG VisUCyte HRP Polymer Antibody (Catalog # VC003) and DAB chromogen (yellow-brown). Tissue was counterstained with hematoxylin (blue). Specific staining was localized to glandular cells.

<b>Genetic Strategies Validation and Orthogonal Strategies Validation.</b>HSKMCs were transfected with scrambled siRNA (scr siRNA) or ABCA1 siRNA. The cells were lysed and ABCA1 (A) protein levels were quantified by immunoblotting. Image collected and cropped by CiteAb from the following publication (//www.nature.com/articles/s41598-018-38014-3) licensed under under a CC-BY license.

<b>Biological Strategies Validation. </b>Analysis of ABCA1 in total cell lysates of RAW264.9 cells treated with vehicle (-) or 9-cisretinoic acid and 22Rhydroxycholesterol (+). Samples used for this testing were 40 ug of total cell post-nuclear lysate from each group.

<b>Biological Strategies Validation. </b>HepG2 cells were grown to 60% confluency, serum starved for 24 hours, and then treated with 1uM TO9 for 24 hours prior to being fixed for 10 minutes using 10% formalin and then permeabilized for 5 minutes using 1X TBS + 0.5% Triton-X100. The cells were incubated with anti-ABCA1 at 5.0ug/ml overnight at 4C and detected with an anti-rabbit Dylight 488 (Green) at a 1:500 dilution. Alpha tubulin (DM1A) NB100-690 was used as a co-stain at a 1:1000 dilution and detected with an anti-mouse Dylight 550 (Red) at a 1:500 dilution. Nuclei were counterstained with DAPI (Blue). Cells were imaged using a 40X objective.

Untreated HepG2 cells were grown to 60% confluency, and serum starved for 24 hours prior to being fixed for 10 minutes using 10% formalin and then permeabilized for 5 minutes using 1X TBS + 0.5% Triton-X100. The cells were incubated with anti-ABCA1 at 5.0ug/ml overnight at 4C and detected with an anti-rabbit Dylight 488 (Green) at a 1:500 dilution. Alpha tubulin (DM1A) NB100-690 was used as a co-stain at a 1:1000 dilution and detected with an anti-mouse Dylight 550 (Red) at a 1:500 dilution. Nuclei were counterstained with DAPI (Blue). Cells were imaged using a 40X objective.

ABCA-1 FITC conjugated antibody of human adipose tissue macrophage subsets by flow cytometry. Image from verified customer review.

Association between expression of ABCA1 and survival in ovarian cancer patients. Expression of ABCA1 in 55 ovarian cancer patient samples was determined by IHC in tissue microarray. Representative image of ovarian cancer showing high (left panel) and low (right panel) ABCA1 expression on the cell membrane or cytoplasm (x400). Image collected and cropped by CiteAb from the following publication (//www.clinicalepigeneticsjournal.com/content/7/1/1), licensed under a CC-BY license.

ABCA1 in human primary fibroblasts in culture. 10 ug of total protein. 7.5% TGX gel. Blocking 5% milk in PBST 1h RT. 1:1000 primary ab in BSA 3% PBST O/N at 4C. Secondary 1:5000 HRP 1h RT. Arrow shows around 250 kDa. WB image submitted by a verified customer review.

ABCA1 antibody was tested at 1: 400 in HeLa cells using an Alexa Fluor 488 secondary (shown in purple). M1 is defined by unstained cells.

<b>Biological Strategies Validation. </b>Detection of ABCA1 in mouse peritoneal macrophages using NB 400-105 (Lot L). ECL exposure, 1 min. Lane 4: T09 uninduced lysate Lane 5: T09 induced lysate.

Prostates of LXR mutant mice accumulate cholesterol esters through inappropriate LXR target genes regulation. Total protein lysates of WT and LXR null mice under normal or high cholesterol diet were analyzed by western blotting with antibodies against ABCA1, LDLR and ACTIN as a loading control (left panel), quantification of ABCA1 and LDLR protein accumulation levels (right panel). * p<0.05, *** p<0.001 in Student's t test. Error bars represent the +/- mean SEM. Image collected and cropped by CiteAb from the following publication (//dx.plos.org/10.1371/journal.pgen.1003483), licensed under a CC-BY license.

miR-33b reduces cellular cholesterol efflux and serum HDL-C levels. Western blotting for ABCA1 (using NB400-105) and ABCG1 proteins in peritoneal macrophages from WT and KI+/+ mice. Representative images are shown. beta-actin was used as the loading control. Image collected and cropped by CiteAb from the following publication (//www.nature.com/articles/srep05312), licensed under a CC-BY license.

miR-33b regulates ABCA1 and SREBP-1. Analysis for ABCA1, SREBP-1, CPT1a, and AMPK alpha protein levels in the livers of WT, KI+/-, and KI+/+ mice. Representative images are shown. TF2B and beta-actin were used as loading controls. Image collected and cropped by CiteAb from the following publication (//www.nature.com/articles/srep05312), licensed under a CC-BY license.

Detection of ABCA1 in human prostate epithelium showing luminal and membrane staining.

Liver mRNA & protein expression analysis of chow-fed Osbpl8KO mice.A: qPCR analysis of the quantity of the mRNAs identified at the bottom in chow-fed KO females (open bars) & males (closed bars). The mRNAs were quantified using ribosomal protein 36B4 message as a housekeeping reference. The data are expressed relative to quantity in littermate WT animals of the same gender, & represent mean ± s.e.m. (n = 6; *p<0.05, **p<0.01, T-test). B: Western blot analysis of ABCA1 & SR-B1 proteins in WT & KO mouse liver. The blots were probed with anti-beta -actin as a loading control. Densitometric quantification of the Western blot data is shown on the right. The results were normalized against beta -actin. The data represents mean ± s.e.m. (n = 4). Image collected & cropped by CiteAb from the following publication (//dx.plos.org/10.1371/journal.pone.0058856), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Protein expressions of ABCA1, SR-BI & ABCG1 in liver & macrophage by Western blot. Simvastatin increased the expressions of ABCA1 & ABCG1 in liver & ABCA1 in macrophage, Both L-4F & the combination group improved the expressions of ABCA1, SR-BI & ABCG1 in liver & ABCA1 & ABCG1 in macrophage. 1P < 0.05, 2P < 0.001, vs. AS group; aP < 0.05, bP < 0.001, vs. Simva group;*P < 0.05, **P < 0.001, vs. L-4F group. Image collected & cropped by CiteAb from the following publication (//lipidworld.biomedcentral.com/articles/10.1186/1476-511X-12-180), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

ABCA1, ABCG1 & SR-BI protein expressions. a & b Hepatic protein expressions of ABCA1, ABCG1 & SR-BI were significantly decreased in COMT−/− mice at GD 18.5, compared to C57BL/6 J mice. Decreased hepatic ABCA1 expression was also observed at 10 days postpartum. ATI-5261 increased ABCA1 & ABCG1 expression in the liver at 10 days postpartum. c Placental protein expressions of ABCA1 & ABCG1 was reduced in COMT−/− mice, compared to C57BL/6 J mice. ATI-5261 treatment significantly increased ABCA1 levels in the placenta of COMT−/− mice. d Representative immunoblots of the corresponding proteins in the placenta with mouse RAW264.7 cell lysate included as positive control. Similar results were obtained when the experiment was repeated with lysates prepared from three batches of tissues. Data are presented as mean ± SEM. Groups (n = 8 in all groups) were compared using one-way ANOVA with post-hoc analysis (Tukey’s procedure). *, p < 0.05 Image collected & cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/30237900), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Effects of 13-HODE & LA in the presence & absence of PPAR alpha & PPAR gamma selective antagonists on molecular markers of cholesterol homeostasis in RAW264.7 macrophages. RAW264.7 cells were pre-treated without or with the PPAR alpha selective antagonist GW6471 or the PPAR gamma selective antagonist GW9662 & subsequently treated without (vehicle control) or with 2.5 μmol/L 13-HODE or 100 μmol/L LA for 24 h. Afterwards, cells were lysed & subsequently processed for western blotting as described in the materials & methods section. A, Representative immunoblots specific for ABCA1, ABCG1, SR-BI, LXR alpha , & beta -actin which was used for normalization are shown. B, Bars represent data from densitometric analysis & are means ± SD from three independent experiments (n = 3). Data are expressed as percentage of protein concentration of vehicle control cells. Results from statistical analysis are indicated: Significant effects are denoted with superscript letters. Bars marked without a common superscript letter significantly differ (P < 0.05). Image collected & cropped by CiteAb from the following publication (//lipidworld.biomedcentral.com/articles/10.1186/1476-511X-10-222), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Western Blot: ABCA1 Antibody - BSA Free [NB400-105] - (A) Upregulation of ABCA1 & ABCG1 & (B) enhancement of cholesterol efflux by purple Perilla frutescens extracts (PPE) in 50 μg/ml Cu2+-oxidized low-density lipoproteins (LDL)-exposed J774A.1 murine macrophages. (A) For the measurement of ABCA1 & ABCG1 expression, total cell lysates were subjected to western blot analysis with a primary antibody against ABCA1 or ABCG1. beta -actin was used as an internal control. Bar graphs (means ± SEM, n=3) represent quantitative densitometric results of the upper bands. (B) Cholesterol efflux was expressed as the percentage of fluorescence in the medium relative to the total fluorescence. Bar graphs denoted without a common letter indicate significant difference, P<0.05. Image collected & cropped by CiteAb from the following publication (//www.spandidos-publications.com/10.3892/ijmm.2015.2101), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Western Blot: ABCA1 Antibody - BSA Free [NB400-105] - 6‐Dihydroparadol increases A) ABCA1 & B) ABCG1, but not C) SR‐BI protein levels in cholesterol‐loaded THP‐1‐derived macrophages. THP‐1 cells were differentiated as described in Figure 2, & then loaded with unlabeled cholesterol for 24 h. Cells were treated with increasing concentrations of 6‐dihydroparadol (1–30 μm) for another 24 h. The protein levels of ABCA1, ABCG1, & SR‐B1 were detected by Western blot analysis. The control was treated with solvent vehicle (0.1% DMSO). As a positive control, TO901317 (5 μm, 24 h) was used. The bar graphs represent mean ± SD from three independent experiments. *p < 0.05, **p < 0.01, & ***p < 0.001 versus control (determined by Student's t‐test or ANOVA with Bonferroni's post hoc test). Image collected & cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/29802792), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Western Blot: ABCA1 Antibody - BSA Free [NB400-105] - Akt inhibition suppresses mTORC1 activity.BHK-ABCA1 cells were induced overnight with mifepristone (10 nM) & then incubated with DEBC, LY294002 or rapamycin at indicated concentrations for 2 h. Cells were then lysed & analyzed for ABCA1 & phosphorylated S6K by Western blotting. Actin was also blotted as loading control. Image collected & cropped by CiteAb from the following publication (//dx.plos.org/10.1371/journal.pone.0113789), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Western Blot: ABCA1 Antibody - BSA Free [NB400-105] - Reversal of hepatic steatosis by reduction of SREBP-1 levels.(a) Western blotting analysis of SREBP-1 & ABCA1 levels in livers of miR-33+/+Srebf1+/+, miR-33+/+Srebf1+/−, miR-33−/−Srebf1+/+ & miR-33−/−Srebf1+/− mice. Representative western blot images are shown (n=4). Image collected & cropped by CiteAb from following publication (//pubmed.ncbi.nlm.nih.gov/24300912), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Western Blot: ABCA1 Antibody - BSA Free [NB400-105] - 6‐Dihydroparadol increases A) ABCA1 & B) ABCG1 protein stability. THP‐1 cells were differentiated as described in Figure 2. Then cells were loaded with unlabeled cholesterol & treated with 6‐dihydroparadol (10 μm), or solvent vehicle (0.1% DMSO, control) for 24 h. Cells were lysed at different time points (0, 1, 2, 3, 4, & 6 h) after treatment with the protein synthesis inhibitor cycloheximide (CHX, 100 μm). The protein levels of both ABCA1 & ABCG1 were detected by Western blot analysis. The data points represent mean ± SD from three independent experiments. *p < 0.05 & **p < 0.01 versus control at the same time point (determined by Student's t‐test). Image collected & cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/29802792), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Western Blot: ABCA1 Antibody - BSA Free [NB400-105] - Ligand activation of LXR inhibits LPS-induced MAP kinase activation through Abca1 induction.(A–D) Bone marrow-derived macrophages from Lxr alpha −/−Lxr beta −/− & control wild-type mice (A, B), or bone marrow-derived macrophages from myeloid-specific Abca1−/− & control wild-type mice (C, D) were pretreated with GW3965 (1 µM) overnight, followed by stimulation with LPS (10 ng/ml) for 20 min or 1 hr. Whole cell lysates were harvested & protein expression was analyzed by immunoblotting with the indicated antibodies (A, C). Protein expression was quantified by Image Quant TL7.0 (B, D). N = 4–6 per group. *p < 0.05, **p < 0.01, NS, not significant. Error bars represent means ± SEM.DOI://dx.doi.org/10.7554/eLife.08009.012 Image collected & cropped by CiteAb from the following publication (//elifesciences.org/articles/08009), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Western Blot: ABCA1 Antibody - BSA Free [NB400-105] - Western Blotting for ABCA1, as detailed in Supplementary Protocol #5 (Additional file 1). Caco-2 cells cultivated on filter inserts were treated for 48 h with bexarotene (RXR agonist, 5 μM), T0901317 (LXR agonist, 10 μM), GW3965 (LXR agonist, 10 μM) or the vehicle control (DMSO 0.1%). Protein expression was then determined by western blot analysis. Results were normalized for interexperimental variance & then set in relation to the vehicle control. Bar graphs represent mean ± SD from three independent experiments. A representative blot is shown - the bands stem from the same membrane & the vertical line indicates excised irrelevant bands. ns not significant, *P < 0.05, **P < 0.01 versus solvent vehicle (determined by paired t-test) Image collected & cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/32308567), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Western Blot: ABCA1 Antibody - BSA Free [NB400-105] - Expression of ABCA1 & CROT in livers & RIP140 in macrophages is elevated in miR-33−/−Apoe−/− mice compared with miR-33+/+Apoe−/− mice. A, Quantitative real-time PCR analysis of Abca1, Crot, Cpt1a, & Prkaa1in livers from miR-33+/+Apoe−/− & miR-33−/−Apoe−/− mice. Values from miR-33+/+Apoe−/− mice were set at 100%. Values are mean±SE (n=9 to 11each); **P<0.01. B, Western analysis of ABCA1, CROT, CPT1a, & AMPK alpha in livers from miR-33+/+Apoe−/− & miR-33−/−Apoe−/− mice. beta -actin was used as a loading control. C, Densitometry of ABCA1, CROT, CPT1a, & AMPK alpha in livers from miR-33+/+Apoe−/− & miR-33−/−Apoe−/− mice. Values from miR-33+/+Apoe−/− mice were set at 100%. Values are mean±SE (n=4 each); *P<0.05. D, Total cholesterol, free cholesterol, cholesterol ester, & triglyceride levels in livers of miR-33+/+Apoe−/− & miR-33−/−Apoe−/− mice. Values are mean±SE (n=9 to 11 each). E, HE staining of livers of miR-33+/+Apoe−/− & miR-33−/−Apoe−/− mice at age 20 weeks fed NC. Scale bar: 100 μm. F, Quantitative real-time PCR analysis of Nrip1 (RIP140) in peritoneal macrophages from miR-33+/+Apoe−/− & miR-33−/−Apoe−/− mice. Values from miR-33+/+Apoe−/− mice were set at 100%. Values are mean±SE (n=7 each). G, Western analysis of NRIP1 (RIP140) in peritoneal macrophages from miR-33+/+Apoe−/− & miR-33−/−Apoe−/− mice. GAPDH was used as a loading control. H, Densitometry of NRIP1 (RIP140) in peritoneal macrophages from miR-33+/+Apoe−/− & miR-33−/−Apoe−/− mice. Values from miR-33+/+Apoe−/− mice were set at 100%. Values are mean±SE (n=4 each); *P<0.05. Image collected & cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/23316322), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Western Blot: ABCA1 Antibody - BSA Free [NB400-105] - Basal ABCA1 expression & function in patient-derived iRPEs. (A) Representation of patient-derived iPSC lines & genotypes harboring polymorphisms in ABCA1 that are associated with decreased or increased risk for AMD development. (B) Relative expression of ABCA1 mRNA in patient-derived iRPEs under basal conditions normalized to RPL28 & decreased risk group. (C) Western blot analysis of ABCA1 levels in patient-derived iRPEs under basal conditions. Actin was detected as loading control. ABCA1 expression was quantified & normalized to actin. (D,E) Relative expression of ABCG1 (D) & NR1H3 (E) mRNA in patient-derived iRPEs under basal conditions normalized to RPL28 & decreased risk group. (F) Cholesterol efflux in patient-derived iRPEs after direct cell labeling & in the presence of ApoAI. (G) Cholesterol efflux in patient-derived iRPEs after phagocytosis of BODIPY-cholesterol-loaded POSs & in the presence of ApoAI. (H) Quantification of phagocytosed POSs per nuclei in patient-derived iRPEs. Values shown are means ± SD (n = 3). * p < 0.05; *** p < 0.001. Unpaired Student’s t-test. (I) Representative fluorescence microscopy images of phagocytosed FITC-labeled POSs (green) & staining for ZO-1 (red) & DAPI (blue) of increased risk cell line IPS19-00096. Scale bar = 100 μm. Image collected & cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/35328615), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Western Blot: ABCA1 Antibody - BSA Free [NB400-105] - A–C) Effects of 6‐dihydroparadol & specific proteasomal, lysosomal, & calpain inhibitors on the ABCA1 protein levels. THP‐1 cells were differentiated as described in Figure 2, & then loaded with unlabeled cholesterol for 24 h. Cells were treated with or without 6‐dihydroparadol (6‐DP, 30 μm) for 24 h & incubated for another 3 h with or without the proteasome inhibitor lactacystin (10 μm), the lysosomal inhibitor chloroquine (100 μm), or the calpain inhibitor calpeptin (30 μg mL−1). The ABCA1 protein levels were detected by Western blot analysis. The bar graphs represent mean ± SD from three independent experiments. *p < 0.05, **p < 0.01, & ***p < 0.001 versus control; n.s., not significant versus control (determined by Student's t‐test or ANOVA with Bonferroni's post hoc test). Image collected & cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/29802792), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Western Blot: ABCA1 Antibody - BSA Free [NB400-105] - Suppressive effects of Ucn1 on foam cell formation & related protein expression in human monocyte-derived macrophages.Human monocytes were incubated for 7 days with RPMI-1640 supplemented with 10% human serum & the indicated concentrations of Ucn1, followed by a 19 h-incubation with 50 µg/ml oxLDL in the presence of 0.1 mmol/l [3H]oleate. Intracellular CE accumulation was determined from the radioactivity of cholesterol-[3H]oleate. Otherwise, before the addition of oxLDL, cells were harvested & subjected to immunoblotting analyses for CD36, ACAT1, or ABCA1. beta -Actin served as a loading control. Data are expressed as means ± SEM from 4–6 independent experiments with monocytes from 4–6 different donors. Baseline (1 fold) = 8.4±2.2 nmol/mg cell protein. *P<0.05, †P<0.001 vs. 0 nmol/l of Ucn1. Image collected & cropped by CiteAb from the following publication (//dx.plos.org/10.1371/journal.pone.0110866), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Western Blot: ABCA1 Antibody - BSA Free [NB400-105] - Effect of evodiamine on ABCA1 transcription & the degradation rate of ABCA1 protein. (a) Differentiated THP-1 macrophages were incubated with 10 μM evodiamine or 10 μM pioglitazone as positive control for 24 h. Total RNA was extracted & ABCA1 mRNA expression levels were quantified by qRT-PCR. (b) 293 T cells were transfected with a luciferase reporter construct driven by the human ABCA1 promoter as described in the Materials & Methods section. After transfection, cells were treated with 10 μM Evodiamine or 1 μM T0901317 as positive control for 24 h. (c) Differentiated THP-1 macrophages were incubated for 24 h with (black circle) or without (Veh; white circle) evodiamine (10 μM) & lysed after addition of cycloheximide (CHX; 140 μM) at different time points (0, 10, 20, 40 min). Western blot analysis shows the decline of ABCA1 protein level with cycloheximide in the presence & absence of evodiamine. All data are means ± S.D. (n = 3) vs. solvent vehicle control (DMSO), *p < 0.05, **p < 0.01, n.s. no significance (ANOVA/Bonferroni). Image collected & cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/30038271), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Western Blot: ABCA1 Antibody - BSA Free [NB400-105] - miR-33 deficiency improved cholesterol efflux in macrophages. A, Quantitative real-time PCR analysis of Abca1 & Abcg1 in macrophages from miR-33+/+Apoe−/− & miR-33−/−Apoe−/− mice. Values from miR-33+/+Apoe−/− were set at 100%. Values are mean±SE (n=7 each); ***P<0.001. B, Western blotting analysis of ABCA1 & ABCG1 in thioglycollate-elicited peritoneal macrophages from miR-33+/+Apoe−/− & miR-33−/−Apoe−/− mice. GAPDH was used as a loading control. C, Cholesterol efflux from thioglycollate-elicited peritoneal macrophages in the presence or absence of apoA-I (5 or 10 μg/mL). Values are mean±SE (n=6 each); **P<0.01. D, Cholesterol efflux from thioglycollate-elicited peritoneal macrophages in the presence or absence of HDL-C (50 or 100 μg/mL). Values are mean±SE (n=6 each); **P<0.01. Image collected & cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/23316322), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Western Blot: ABCA1 Antibody - BSA Free [NB400-105] - Srebf1 is a miR-33 target gene.(a) Relative changes in lipid metabolism-related genes in the livers of miR-33−/− mice compared with miR-33+/+ mice fed NC at 16 weeks of age. (n=5–8 each,*P<0.05 in Student’s t-test). (b) Conservation of miR-33 target regions in the 3′UTR of Srebf1. Underlined sequences are the potential binding site of miR-33 seed sequences. * indicates the conservation among spieces. (c) 3′UTR reporter assay used to verify the target. Luciferase reporter activity of human & mouse SREBP-1 gene 3′UTR constructs in 293T cells overexpressing miR-control (miR-Con) & miR-33 (n=4 each, *P<0.05 & ***P<0.001 in Student’s t-test). (d) miR-33 dose-dependent changes in luciferase reporter activity of mouse Srebf1 3′UTR construct in 293T cells. miR-Con & miR-146a is used as a negative control (n=4 each, *P<0.05 & ***P<0.001 in one-way analysis of valiance test). (e) Luciferase reporter activity of the WT or mutant Srebf1 3′UTR at the potential miR-33 binding site in 293T cells (n=4 each, **P<0.01 in Student’s t-test). (f,g) Luciferase reporter activity of SRE-promoter (f) or FAS-promoter (g) in 293T cells. 293T cells were co-transfected with mouse Srebf1 with the full-length 3′UTR or without the 3′UTR, along with expression plasmids for miR-negative control, or miR-33. Values are the mean±s.e. (n=4 each, **P<0.01 versus miR-Con. ***P<0.001 versus miR-Con in one-way analysis of valiance test). (h) Western blotting analysis of SREBP-1, ABCA1, & IRS-2 in miR-33 transduced HepG2 cells & primary hepatocytes & hepatocytes prepared from miR-33+/+ & miR-33−/− mice. Representative western blot images are shown (n=4). Values are the means±s.e.m. Image collected & cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/24300912), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Western Blot: ABCA1 Antibody - BSA Free [NB400-105] - (A) Chemical structure, (B) cytotoxicity of alpha -asarone, (C) enhancement of cholesterol efflux by alpha -asarone, (D & E) upregulation of ABCA1 & ABCG1 by alpha -asarone & beta -asarone, & (F) elevation of retinoid X receptor (RXR) alpha transcription. J774A.1 murine macrophages were exposed to 50 μg/ml oxidized low-density lipoprotein (LDL) & treated with 1–10 μM purple Perilla frutescens extracts (PPE)-alpha -asarone & 5–10 μM beta -asarone. (B) MTT assay was performed for the measurement of alpha -asarone toxicity. Graph data represent 1 of 4 independent experiments with multiple estimations. Values are expressed as the percentage cell survival relative to the untreated control cells (cell viability, 100%). (C) Cholesterol efflux was expressed as the percentage fluorescence in the medium relative to total fluorescence. (D & E) For the measurement of ABCA1 & ABCG1 expression, total cell lysates were subjected to western blot analysis with a primary antibody against ABCG1 or ABCG1. beta -actin was used as an internal control. Bar graphs (means ± SEM, n=3) represent quantitative densitometric results of the upper bands. Bar graphs denoted without a common letter indicate significant difference, P<0.05. (F) RXR alpha mRNA expression was measured by RT-PCR. GAPDH was used as a housekeeping gene for the co-amplification with RXR alpha . Image collected & cropped by CiteAb from the following publication (//www.spandidos-publications.com/10.3892/ijmm.2015.2101), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Western Blot: ABCA1 Antibody - BSA Free [NB400-105] - Bilirubin significantly decreases expression of ATP‐binding cassette transporter A1 (ABCA1) protein in THP‐1 macrophages treated with LXR agonist (TO901317) to upregulate ABCA1 protein. THP‐1 cells were differentiated for 72 hours with 200 nmol/L phorbol‐12‐myristate‐13‐acetate & then loaded with unlabeled cholesterol for another 24 hours. Cells were treated with TO901317 (5 μmol/L) or solvent vehicle (0.1% dimethyl sulfoxide [DMSO]) for 24 hours. Afterward, cells were treated with bilirubin (17.1 μmol/L) or solvent vehicle (0.1% DMSO) for 16 hours. The protein levels of ABCA1 were detected by western blot analysis. The bar graphs present mean±SD from 3 independent experiments. ***P<0.001 vs control (determined by ANOVA with Bonferroni post hoc test). Image collected & cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/28455345), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Western Blot: ABCA1 Antibody - BSA Free [NB400-105] - Induction of cholesterol efflux attenuates the enhancement in HIV-1infectivity in NPCD55 cells. (A) Normal & NPCD55 cells were treated with 5 μM TO-901317 at 24 h post-infection & cultured for 72 h in the presence of the compound. At 96 h post-infection the cells were harvested & ABCA1, Gag, & beta -actin expression was detected by Western blotting analysis. All samples were loaded on the same gel. (B) AmplexRed assay was performed to measure free cholesterol content of untreated (filled) & TO-901317-treated (slashed) cells. Cholesterol content was normalized to protein concentration. (C) AmplexRed assay was performed to measure virion-associated cholesterol from purified virus produced in untreated (filled) & TO-901317-treated (slashed) infected cells. Virion-associated cholesterol content was normalized to p24 concentration. (D) TZM-bl reporter assay was performed to measure virus infectivity when cholesterol efflux was induced via TO-901317 stimulation. The ρ values were calculated by performing student T-test (*denotes < 0.05). Image collected & cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/22273177), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Western Blot: ABCA1 Antibody - BSA Free [NB400-105] - Effects of apabetalone on ABCA1 expression & carboplatin response in ovarian cancer cells. (A) Apabetalone treatment reduced expression of ABCA1 in OVCAR-5 & OVCAR-5 CBPR cell lines. Cells were treated for 72 h with control medium (DMSO) or apabetalone (80 µM). Protein extracts from OVCAR-5 (~30 µg) were electrophoresed & immunoblotted with rabbit polyclonal ABCA1 antibody (1/1000, NB400-105, Novus Biological) & beta -actin (1/2000, Abcam) was used as a loading control. (B) Quantification of Western blot. OVCAR-5 (C), CaOV3 (D), OVCAR-5 CBPR (E) & CaOV3 CBPR (F) cell survival following treatment with carboplatin (CBP) alone (0-200 µM, black line) & in combination with apabetalone (Apa, 80 µM, purple line). (G) Carboplatin IC50 for OVCAR-5 & OVCAR-5 CBPR cells ± apabetalone. Data are mean ± SEM from three independent experiments. *P < 0.05, Student’s t-test. (H) Carboplatin IC50 for CaOV3 & CaOV3 CBPR cells ± apabetalone. Data are mean ± SEM from three independent experiments. P < 0.05, Student’s t-test. Image collected & cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/35582032), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Western Blot: ABCA1 Antibody - BSA Free [NB400-105] - Expression of ATP‐binding cassette transporter A1 (ABCA1) protein in THP‐1 macrophages treated with bilirubin & in peripheral blood mononuclear cells (PBMCs) from Gilbert syndrome (GS) patients. A, Bilirubin suppresses the expression of ABCA1 protein in THP‐1‐derived macrophages time‐dependently. THP‐1 cells were differentiated as described in Figure 1 & then loaded with unlabeled cholesterol for another 24 hours. Cells were treated with bilirubin (17.1 μmol/L) for 4, 8, 16, & 24 hours. The protein levels of ABCA1 were detected by western blotting. Control was treated with solvent vehicle (0.1% dimethyl sulfoxide). The bar graph presents mean±SD from 3 independent experiments. B, Expression of ABCA1 protein is decreased in PBMCs from participants with high bilirubin blood levels (GS) compared with healthy controls. The protein levels of ABCA1 were detected by western blotting. The bar graph presents mean±SEM (n=28 per group). *P<0.05, **P<0.01 & ***P<0.001 vs control. ns indicates not significant (determined by Student t test). Image collected & cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/28455345), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Western Blot: ABCA1 Antibody - BSA Free [NB400-105] - (A) Time course response of ABCA1 induction by pioglitazone, & (B) enhancement of ABCA1 & (C) peroxisome proliferator-activated receptor gamma (PPAR gamma ) by purple Perilla frutescens extracts (PPE). J774A.1 murine macrophages were incubated with 10 μM pioglitazone & 50 μg/ml oxidized low-density lipoprotein (LDL) in the absence or presence of 1–10 μg/ml PPE. For the measurement of expression of (A & B) ABCA1 & (C) PPAR gamma , total cell lysates were subjected to western blot analysis with a primary antibody against ABCA1 or PPAR gamma . beta -actin was used as an internal control. Bar graphs (means ± SEM, n=3) represent quantitative densitometric results of the upper bands. Bar graphs denoted without a common letter indicate significant difference, P<0.05. Image collected & cropped by CiteAb from the following publication (//www.spandidos-publications.com/10.3892/ijmm.2015.2101), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Western Blot: ABCA1 Antibody - BSA Free [NB400-105] - LXR agonist-stimulated ABCA1 expression & function in patient-derived iRPEs. Patient-derived iRPE lines were stimulated for 16 h with LXR agonist & are relative to unstimulated cells shown in Figure 2. (A) Expression of ABCA1 mRNA normalized to RPL28 & relative to unstimulated cells shown in Figure 2B. (B) Western blot analysis of ABCA1 protein levels. Actin was detected as loading control. ABCA1 expression was quantified & normalized to actin. (C) Cholesterol efflux assay after direct cell labeling & in the presence of ApoAI. (D) Cholesterol efflux assay after phagocytosis of BODIPY-cholesterol-loaded POSs & in the presence of ApoAI. Data are relative to unstimulated cells shown in Figure 2F,G, respectively. Data are presented as means ± SD (n = 3). Unpaired Student’s t-test. * p < 0.05. Image collected & cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/35328615), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Western Blot: ABCA1 Antibody - BSA Free [NB400-105] - Akt inhibition by LY294002 or Akt1/2 also enhances cholesterol efflux to apoA-I from ABCA1-expressing BHK cells.A) BHK cells were induced as in Fig. 1 & then incubated with LY294002 (200 µM) for 2 h. Cells were then lysed & analysed for ABCA1, phosphorylated Akt (p-Akt) & total Akt by Western-blotting. Hsp70 was also blotted as loading control. B & C) BHK cells were labeled with [3H] cholesterol & induced with 10 nM mifepristone overnight. Cholesterol efflux was measured after 2 h incubation with BSA (1 mg/ml) or BSA plus apoA-I (5 µg/ml). Some of cells were also incubated with indicated doses of LY294002 (B) or Akt1/2 (C), in addition to apoA-I, during 2 h efflux period. Results are presented as the average of triplicate wells with standard deviation & representative of more than three independent experiments. *** P<0.0001, **P<0.001 & *P<0.05 vs apoA-I only. Image collected & cropped by CiteAb from the following publication (//dx.plos.org/10.1371/journal.pone.0113789), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Western Blot: ABCA1 Antibody - BSA Free [NB400-105] - Generation, differentiation & analysis of ABCA1-deficient iRPEs. (A) Immunofluorescence staining for ZO-1 (red) in 4-week cultured iRPEs. Nuclei were stained with DAPI (blue). Scale bar = 100 μm. (B) Bright-field microscopy of iRPEs. (C) Ct values of RPE marker genes BEST1, OTX2, RLBP1 & RPE65 in iRPEs & parental iPSCs obtained by qPCR. Values shown are means ± SD (n = 3). Unpaired Student’s t-test. **** p < 0.0001. (D) Sequence alignment of parts of exon 14 (top) & exon 46 (bottom) of ABCA1-deficient iRPE cell clones & parental line. (E) Western blot of ABCA1 protein levels in ABCA1-deficient iRPE cell lines & parental cell line after 16 h of stimulation with 1 μM LXR agonist. Actin was detected as loading control. (F) Relative expression of ABCA1 mRNA in ABCA1-deficient iRPE cell lines & parental cell line normalized to ACTB. Values shown are means ± SD (n = 3). One-way ANOVA with Tukey’s post hoc test. **** p < 0.0001. (G) Relative expression of ABCG1 mRNA in ABCA1-deficient iRPE cell lines & parental cell line normalized to ACTB. Values shown are means ± SD (n = 3). One-way ANOVA with Tukey’s post hoc test. ** p < 0.01; *** p < 0.001. (H) Cholesterol efflux assay in iRPEs in the presence of ApoAI and/or LXR agonist (LXR ag). Values shown are means ± SD (n = 3). Two-way ANOVA with Bonferroni post hoc test vs. DMSO + BSA control. **** p < 0.0001. (I) Bright-field (BF) microscopy & Nile Red fluorescence microscopy (overview & close-up view marked with white squares) of 4-week cultured ABCA1-deficient iRPE cell lines & parental cell line. Relative fluorescence was quantified & is shown as mean ± SD (n = 8). One-way ANOVA with Tukey’s post hoc test. * p < 0.05, **** p < 0.0001. Image collected & cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/35328615), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Western Blot: ABCA1 Antibody - BSA Free [NB400-105] - Akt inhibition enhances cholesterol efflux to apoA-I from wt MEFs, but not from TSC2-/- MEFs where mTORC1 is constitutively activated.A) Mouse embryonic fibroblasts (MEFs), wt & TSC2-/-, were induced overnight with T0901317 (10 µM). Cell lysates were collected for Western blotting for phosphorylated S6K & total S6K. B) wt & TSC2-/- MEFs were incubated with or without T0901317 (10 µM) overnight. Some of cells were then incubated with apoA-I (10 µg/ml) or apoA-I plus DEBC (25 µM) for 2 h. The expression of ABCA1, phosphorylated Akt, total Akt & loading control hsp70 were analyzed by Western blotting. C) wt & TSC2-/- were labeled with [3H] cholesterol for 1 day & then incubated with or without T0901317 (10 µM) overnight. Some of cells were then incubated with apoA-I (10 µg/ml) or apoA-I plus DEBC (25 µM) for 2 h to analyze cholesterol efflux. Data presented as the average of triplicate wells with standard deviation & representative of at least three independent experiments. *** P<0.0001 vs apoA-I only. Image collected & cropped by CiteAb from the following publication (//dx.plos.org/10.1371/journal.pone.0113789), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Western Blot: ABCA1 Antibody - BSA Free [NB400-105] - Akt inhibition by DEBC enhances cholesterol efflux to apoA-I specifically from ABCA1-expressing BHK cells.A) BHK-ABCA1 cells were induced with mifepristone (10 nM) overnight & then incubated with indicated doses of DEBC for 2 h. Cells were then lysed & Western-blotted for ABCA1, phosphorylated Akt (p-Akt) & total Akt. Hsp70 was also blotted as loading control. B) BHK-ABCA1 cells were labeled with [3H] cholesterol & induced overnight as above. After 2 h incubation with BSA (1 mg/ml) or BSA plus apoA-I (5 µg/ml), cholesterol efflux was measured as described in the Methods section. Some of the cells were also incubated with indicated doses of DEBC, in addition to apoA-I, during 2 h efflux period. C) BHK-ABCA1 & BHK-A937V cells were induced with mifepristone (10 nM) overnight. 2 h Cholesterol efflux was measured as above either with or without DEBC (25 µM). Results are presented as the average of triplicate wells with standard deviation & representative of more than three independent experiments. *** P<0.0001 & **P<0.001 vs apoA-I only. Image collected & cropped by CiteAb from the following publication (//dx.plos.org/10.1371/journal.pone.0113789), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Western Blot: ABCA1 Antibody - BSA Free [NB400-105] - LXRs control expression of genes involved in cholesterol homeostasis & fatty acid synthesis in MPECs.(A) qPCR analysis of Abca1, Abcg1 & Idol levels in WT (+/+) & Lxr alpha beta −/− (lxr−/−) MPECs after DMSO (vehicle) or T0901317 stimulation (B) Effect of 9-cis retinoic acid and/or T0901317 stimulation on Abca1 accumulation levels in WT (+/+) & Lxr alpha beta −/− (lxr−/−) MPECs (C) qPCR analysis of Srebp1, Acc, & Fas levels in WT (+/+) & Lxr alpha beta −/− (lxr−/−) MPECs after DMSO (vehicle) or T0901317 stimulation. (qPCR analysis results from 4 independant experiments & was normalized using 36b4 gene). *p<0.05, **p<0.01, ***p<0.001 in Student’s t test. Error bars represent mean ± SEM. (D) Western blot analysis was performed on WT (+/+) or Lxr alpha beta −/− MPECs using Srebp1c, Abca1 & beta -Actin antibodies. (E) Oil-Red O staining (ORO) & Normarski/Dapi of WT (+/+) & Lxr alpha beta −/− MPECs, or WT MEFs, treated for 48h with DMSO (vehicle) or T0901317 (1 µM). Head arrows indicate lipid droplets. Scale bars 100 µm. Image collected & cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/23554947), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Western Blot: ABCA1 Antibody - BSA Free [NB400-105] - Anti-ApoA-1 IgGs upregulate ABCA1. ABCA1 was increased after 16 & 24 h of anti-ApoA-1 IgG exposure to HMDM at the mRNA level as revealed by RT-PCR (a) as well as at the protein level after 24 h anti-apoA-1 IgG stimulation, as revealed by Western blot analysis (b). In panel a, data are expressed as fold change expression of the mean ± SD of ABCA1 calculated by delta delta CT method of six independent experiments (n = 6) & values were normalized to untreated condition. p-values were calculated using the Student’s t-test: * p < 0.05, ** p < 0.01, **** p < 0.0001. (b) One of four representative Western blots is shown. Data are the mean ± SD of band intensity volume/actin intensity volume of four independent experiments (n = 4). p-values were calculated using the Student’s t-test: * p = 0.02, ** p = 0.005. Image collected & cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/31766415), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Western Blot: ABCA1 Antibody - BSA Free [NB400-105] - ABCA1 protein expression is upregulated in ovarian cancer cells with acquired carboplatin resistance. ABCA1 expression in OVCAR-5 (A) & CaOV3 (C) & carboplatin resistant OVCAR-5 CBPR (B) & CaOV3 CBPR (D) by immunocytochemistry using rabbit polyclonal ABCA1 antibody (1/100, NB400-105, Novus Biological). (E) OVCAR-5 cells with Rabbit IgG & (F) CaOV3 cells with Rabbit IgG. (G) Protein extracts from OVCAR-5 (~30 µg) & CaOV3 cell lines (~60 µg) were electrophoresed & immunoblotted with rabbit polyclonal ABCA1 antibody (1/1000, NB400-105, Novus Biological), & beta -actin (1/2000, Abcam) was used as a loading control. A major band was detected at ~250 kDa, which is the predicted size for ABCA1. (H) Quantitation of ABCA1 Western blots. Data are from 2-4 independent experiments. Statistical significance was determined using the Student’s t-test, *P < 0.05. Image collected & cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/35582032), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Western Blot: ABCA1 Antibody - BSA Free [NB400-105] - Evodiamine enhances apo A1-mediated ChE from THP-1 macrophages & increases ABCA1 protein level. (a) Differentiated THP-1 cells were loaded with [3H]-cholesterol together with the indicated treatments for 24 h. On the next day, the cells were washed twice with PBS & incubated with the same compounds [solvent vehicle control (Veh; ≤0.1% DMSO), evodiamine (1–20 μM), & the PPAR gamma agonist pioglitazone (10 μM) as positive control] with or without 10 µg/mL apo A1. Extracellular as well as intracellular radioactivities were quantified with scintillation counter. Differentiated THP-1-derived macrophages were treated with solvent vehicle control (Veh; ≤0.1% DMSO), evodiamine (10 μM), & the PPAR gamma agonist pioglitazone (10 μM) as positive control. After 24 h incubation, the cells were lysed & 20 μg protein was resolved via SDS-PAGE. Immunodetection was performed with antibodies against the indicated proteins, ABCA1 (b), ABCG1 (c), & SR-B1 (d), & visualized by chemiluminescence detection. All experiments were performed at least three times & data are presented as means ± S.D. vs. solvent vehicle control, *p < 0.05, **p < 0.01, ***p < 0.001, n.s. no significance (ANOVA/Bonferroni). Image collected & cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/30038271), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Western Blot: ABCA1 Antibody - BSA Free [NB400-105] - Functional miR-33 responsive elements in the 3′UTR of ATP8B1 & ABCB11A,B. Conserved sequences in the 3′UTR of ATP8B1 & ABCB11 are partially complementary to miR-33. The element in human ATP8B1 is located 1877–1897 nt after the stop codon. The element in ABCB11 overlaps the stop codon in primates, while rodents show a conserved sequence 732–751 nt after the stop codon.C,D. Luciferase assays in HEK293 cells using the whole 3′UTR of human or murine ATP8B1 & ABCB11, or a single copy of the responsive elements (RE) identified above, or mutant responsive elements (RE*; where AATGCA was mutated to GGGTTG to prevent complementarity to the seed sequence of the miRNA), co-transfected with (closed bars) or without (open bars) a vector to overexpress miR-33. In grey, data from empty (negative control) & R33 (positive control containing a 100% match to miR-33) reporter vectors.E,F. Relative mRNA expression of canalicular transporters in primary murine hepatocytes (n = 4 dishes/condition) & human HuH-7 hepatoma cells (n = 3 dishes/condition) transduced 48 h with empty or miR-33 adenovirus.G. Relative protein levels in HuH7 cells transduced with empty or miR-33 adenovirus. Some cells were incubated for 16 h in the presence of FXR:RXR agonists (2 µmol/L GW4064 : 1 µmol/L 9-cis-retinoic acid) to induce ABCB11. Asterisk indicates a non-specific band. Data shown as mean ± SD; **p < 0.01. Image collected & cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/22767443), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Western Blot: ABCA1 Antibody - BSA Free [NB400-105] - Gas6 treatment enhances expression of LXR alpha & LXR beta & their target genes in BMDM.Mouse BMDM were stimulated with 400 ng/ml Gas6, 1 μM T0901317, 10 ng/ml interferon (IFN)-gamma , 10 ng/ml IL-4, or 100 ng/ml LPS for 4 h (a,b) or 400 ng/ml Gas6 for the indicated times (c–g). (a,b,e) The amounts of the LXR alpha , LXR beta , ABCA1, ABCG1, ApoE, AIM, Arg2, VEGF, YM1, & Arg1 mRNAs were analyzed by real-time PCR & normalized to that of Hprt mRNA. (c,d,f,g) The relative abundances of LXR alpha , LXR beta , ABCA1, ABCG1, ApoE, Aim, Arg2, & VEGF proteins were determined by Western blotting analysis. The relative densitometric intensity was determined for each band & normalized to beta -actin. Data in all bar graphs are means ± SEM of three independent experiments. *P < 0.05 compared with control. Image collected & cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/27406916), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Western Blot: ABCA1 Antibody - BSA Free [NB400-105] - (A) Time course response of ABCA1 induction by TO-091317 & (B) upregulation of ABCA1 by purple Perilla frutescens extracts (PPE), & (C) enhancement of liver X receptor (LXR) alpha induction by PPE. J774A.1 murine macrophages were cultured with 1 μM TO-091317 or 50 μg/ml Cu2+-oxidized low-density lipoprotein (LDL) in the absence or presence of 1–10 μg/ml PPE. For the measurement of expression of (A & B) ABCA1 & (C) LXR alpha , total cell lysates were subjected to western blot analysis with a primary antibody against ABCA1 or LXR alpha . beta -actin was used as an internal control. Bar graphs (means ± SEM, n=3) represent quantitative densitometric results of the upper bands. Bar graphs denoted without a common letter indicate significant difference, P<0.05. Image collected & cropped by CiteAb from the following publication (//www.spandidos-publications.com/10.3892/ijmm.2015.2101), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Reactivity:

Hu, Mu, Rt, Po, Ca, Ch, ChHa, Eq, Ha, Md, Pm, Rb

Species Glossary

Reactivity: Hu, Mu, Rt, Po, Ca, Ch, ChHa, Eq, Ha, Md, Pm, Rb

Applications:

, , , , , , , , , , , , , , , ,

Applications: , , , , , , , , , , , , , , , ,

Host:

Rabbit Polyclonal

Host: Rabbit Polyclonal

Sizes:

Sample Size Available

Sizes: Sample Size Available

Conjugate:

Unconjugated

Available Conjugates:

Validated by:

Validated by:

Conjugate	Catalog #	Availability	Size	Price
Alexa Fluor 350	NB400-105AF350
Alexa Fluor 405	NB400-105AF405
Alexa Fluor 488	NB400-105AF488
Alexa Fluor 532	NB400-105AF532
Alexa Fluor 594	NB400-105AF594
Alexa Fluor 647	NB400-105AF647
Alexa Fluor 700	NB400-105AF700
Alexa Fluor 750	NB400-105AF750
Allophycocyanin	NB400-105APC
Allophycocyanin/Cy7	NB400-105APCCY7
Biotin	NB400-105B
CoraFluor 1	NB400-105CL1
DyLight 350	NB400-105UV
DyLight 405	NB400-105V
DyLight 488	NB400-105G
DyLight 550	NB400-105R
DyLight 594	NB400-105DL594
DyLight 650	NB400-105C
DyLight 680	NB400-105FR
DyLight 755	NB400-105IR
FITC	NB400-105F
HRP	NB400-105H
Janelia Fluor 525	NB400-105JF525
Janelia Fluor 549	NB400-105JF549
Janelia Fluor 646	NB400-105JF646
Janelia Fluor 669	NB400-105JF669
PE	NB400-105PE
PE/Atto594	NB400-105PEATT594
PE/Cy5.5	NB400-105PECY55
PE/Cy7	NB400-105PECY7
PerCP	NB400-105PCP
mFluor Violet 450 SE	NB400-105MFV450
mFluor Violet 500 SE	NB400-105MFV500
mFluor Violet 610 SE	NB400-105MFV610

Available Formulations

Formulation	Catalog #	Availability	Price
BSA Free	NB400-105SS

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NB100-2323

IRE1 alpha [p Ser724] Antibody - BSA Free

(9 Reviews)

(372 Publications)

0.1 ml

NB100-2323

P-Ire1a activation correlates with WFS1 cell expression. Cryosections of retina from 12 month old Wfs1+/+ and Wfs1-/- mouse were immunostained with anti-P-Ire1a antibody (red). DAPI was used for staining of cell nuclei (blue). RPE, retinal pigment epithelium; ONL, outer nuclear layer; INL, inner nuclear layer, RGC, retinal ganglion cells. Scale bars=50 um. Image collected and cropped by CiteAb from the following publication (//doi.org/10.1371/journal.pone.0097222) licensed under a CC-BY license.

Hepatic ER stress markers with cachexia progression. ER stress markers Bip, IRE1a, ATF6p50 and CHOP were examined in the liver of non, pre and severely cachectic mice. (n = 6-8 per group, p < 0.05) Dotted line indicates levels of Non-cachectic mice. Non = Non-Cachectic Apc Min/+ Sev = severely cachectic Apc Min/+; * denotes significantly different from Non-cachectic Apc Min/+ Image collected and cropped by CiteAb from the following publication (//doi.org/10.1371/journal.pone.0119888) licensed under a CC-BY license.

IRF-1 plays a central role in ER stress-mediated modulation of VCAM-1 expression by TGRL. HAEC were conditioned for 4 hr with TNFa (0.3 ng/ml) E: CHOP knockdown decreased TNFa-induced VCAM-1 expression. n=4. **P<0.01 vs. siCtrl+TNFa. Shown are representative blots from 3 independent experiments with similar results. Image collected and cropped by CiteAb from the following publication (//doi.org/10.1371/journal.pone.0078322) licensed under a CC-BY license.

Analysis using HRP conjugate of NB100-2323. Detection of phosphorylated IRE-1 alpha using NB100-2323. Lane 1: COS-7 untransfected Lane 2: COS-7 expressing wild-type IRE1 alpha Lane 3: COS-7 expressing kinase-dead IRE1 alpha. Theoretical molecular weight: 110 kDa.

<b>Biological Strategies Validation. </b>Analysis of anti-IRE1 alpha (pSer724) using Lot AN and AO of NB100-2323. HeLa cells were treated (+) or untreated (-) with 10 mM DTT for 60 min to activate the UPR. Total protein was separated on a 7.5% gel by SDS-PAGE, transferred to PVDF membrane and blocked in 5% BSA in TBST. The membrane was probed with 2.0 ug/ml antibody in 5% BSA, and detected with an anti-rabbit HRP secondary antibody using chemiluminescence. Theoretical molecular weight: 110 kDa.

Regulation of the unfolded protein response by KLF15. Western analysis of UPR activity in WT versus KLF15-/- primary hepatocytes. Hepatocytes were isolated from standard chow-fed 4-month-old male WT and KLF15 -/- mice. Two individual experiments were performed in triplicate; each lane indicates a technical replicate. Image collected and cropped by CiteAb from the following publication (//doi.org/10.1371/journal.pone.0077851) licensed under a CC-BY license.

HeLa cell lysate, 20 ug. Antibody at 1:1000, 1% skim milk in TBST, overnight incubation at 4C. WB image submitted by a verified customer review.

<b>Biological Strategies Validation. </b>Detection in Min6 cells which were treated with different concentrations of glucose for 3 hours prior to lysates preparation.

IRE1 (pS724) was detected in immersion fixed paraffin-embedded sections of human spleen using Rabbit Anti-Human IRE1 (pS724) polyclonal Antibody (Catalog # NB100-2323) at 1:300 for 1 hour at room temperature followed by incubation with the Anti-Rabbit IgG VisUCyte™ HRP Polymer Antibody (Catalog # VC003). Tissue was stained using DAB (brown) and counterstained with hematoxylin (blue). Specific staining was localized to the perinuclear cytoplasm in splenocytes.

Hepatic ER Stress.Representative hepatic western blots of BiP, phosphorylated (Ser51), total EIF2 alpha and phosphorylated:total EIF2 alpha , phosphorylated (Ser724), total IRE1 alpha and phosphorylated:total IRE1 alpha , and CHOP (n = 9). Diets not sharing a common letter differ significantly from one another (P≤.05).

Morphine suppressed 6-OHDA-induced ER stress through activation of UPR. (A,B) Morphine induced UPR in SH-SY5Y cells. Protein levels of GRP78, p-IRE1 alpha , IRE1 alpha , p-PERK, PERK, ATF6, CHOP and Tubulin in SH-SY5Y cells were analyzed (A) and quantified (B) by western blot. ∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001 vs. control.

Effect of cancer on ER stress markers.Bip1, IRE-1, ATF-6 p50 and CHOP expression in the liver of non—cachectic ApcMin/+ mice (N = 6 per group), compared to healthy C57BL/6 mice. Dotted line on the western blot indicates two different sections of the same gel. Values are expressed as Mean ± SE. * denotes significantly different from the healthy C57BL/6 mice as analyzed by a pre—planned t—test. p < 0.05.

Western Blot: IRE1 alpha [p Ser724] Antibody - BSA Free [NB100-2323] - ABT-263 induces ER stress & activation of the unfolded protein response.a Western blot of ER stress molecules in uveal melanoma cells treated with ABT-263 5 μM for 24 h & 48 h. HSP90 is used as a loading control. Representative western blots are shown. b XBP1 splicing in uveal melanoma cells exposed to ABT-263 5 μM for 15 h. *P-value < 0.05, **P-value < 0.01. c Kinetic analysis of ER stress proteins in Mel270 cells treated with ABT-263 5 μM in the absence or presence of qVD-OPh 20 μM. HSP90 is used as a loading control. Representative western blots are shown. Image collected & cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/32337074), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Western Blot: IRE1 alpha [p Ser724] Antibody - BSA Free [NB100-2323] - Effect of cancer on ER stress markers.Bip1, IRE-1, ATF-6 p50 & CHOP expression in the liver of non—cachectic ApcMin/+ mice (N = 6 per group), compared to healthy C57BL/6 mice. Dotted line on the western blot indicates two different sections of the same gel. Values are expressed as Mean ± SE. * denotes significantly different from the healthy C57BL/6 mice as analyzed by a pre—planned t—test. p < 0.05. Image collected & cropped by CiteAb from the following publication (//dx.plos.org/10.1371/journal.pone.0119888), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Western Blot: IRE1 alpha [p Ser724] Antibody - BSA Free [NB100-2323] - ER stress is induced by acidosis activated OGR1-mediated signalling. Caco-2 cells subjected to different pH medium, following 4–6 h incubation in pH 7.6 serum free medium.(B) After 24 h pH shift, total protein was isolated & WB was performed. The results representative of 3 independent experiments. Image collected & cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/31996710), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Western Blot: IRE1 alpha [p Ser724] Antibody - BSA Free [NB100-2323] - Expression of ER stress markers in mouse & human skeletal muscle(a) TA muscle lysates from high fat fed mice were used to determine the expression of ER stress markers by Western blot analysis (n=6). (b-g) Western blot analysis was done to measure proteins involved in ER stress in vastus lateralis muscle from lean, obese, or diabetic subjects (n=6-13). Data are the means ± S.E.M. * indicates p<0.05 & ** indicates p<0.01 vs. chow or lean controls, using Student’s t-test (a) & One way ANOVA. Image collected & cropped by CiteAb from the following publication (//www.nature.com/articles/ncomms2851), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Western Blot: IRE1 alpha [p Ser724] Antibody - BSA Free [NB100-2323] - The inositol-requiring enzyme 1 alpha (IRE1 alpha )/ X-box-binding-protein 1 spliced isoform (XBP1s) arm of unfolded protein response (UPR) is induced by angiotensin II in VSMCs. (A–C) The rat aortic VSMCs infected with adenovirus encoding GRP78 or control GFP (100 moi) for 48 h were stimulated with 100 nM AngII (AII) for 1–6 h & immunoblotting was performed as indicated. (A) Representative blots from 4 independent experiments. (B) Signal intensity was used to calculate the expression ratio of XBP1s to GAPDH. (C) Signal intensity was used to calculate the IRE1 alpha Ser724 phosphorylation ratio to the total IRE1 alpha . The bars in the graphs show the mean ± SD from 4 independent experiments. * indicates p < 0.05. Image collected & cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/32679678), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Western Blot: IRE1 alpha [p Ser724] Antibody - BSA Free [NB100-2323] - Morphine suppressed 6-OHDA-induced ER stress through activation of UPR. (A,B) Morphine induced UPR in SH-SY5Y cells. Protein levels of GRP78, p-IRE1 alpha , IRE1 alpha , p-PERK, PERK, ATF6, CHOP & Tubulin in SH-SY5Y cells were analyzed (A) & quantified (B) by western blot. ∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001 vs. control. (C,D) Protein levels of GRP78, CHOP & Actin in SH-SY5Y cells were analyzed (C) & quantified (D) by western blot in the indicated groups. ∗P < 0.05, ∗∗P < 0.01 vs. control & #P < 0.05, ##P < 0.01 vs. 6-OHDA-treated group. All data are expressed as mean ± SEM. Image collected & cropped by CiteAb from the following publication (//journal.frontiersin.org/article/10.3389/fnmol.2018.00120/full), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Western Blot: IRE1 alpha [p Ser724] Antibody - BSA Free [NB100-2323] - Hepatic ER Stress.Representative hepatic western blots of BiP, phosphorylated (Ser51), total EIF2 alpha & phosphorylated:total EIF2 alpha , phosphorylated (Ser724), total IRE1 alpha & phosphorylated:total IRE1 alpha , & CHOP (n = 9). Diets not sharing a common letter differ significantly from one another (P≤.05). Image collected & cropped by CiteAb from the following publication (//dx.plos.org/10.1371/journal.pone.0167979), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Western Blot: IRE1 alpha [p Ser724] Antibody - BSA Free [NB100-2323] - Effect of Insig-1 overexpression on nSREBP-1c & proteins related to ER stress pathway in INS-1 cells. INS-1 & INS-1-Insig-1 cells were stimulated with 11.2 mM & 25.0 mM glucose for 0, 24 & 72 h. A) nSREBP-1c & p-IRE1 alpha pathway of ER stress related proteins were detected by Western blot. GAPDH was used as control for protein loading. Equal amount of proteins (50 μg) were loaded. B) Relative protein expression compared to GAPDH, data are the means ± SE of three independent experiments; *, P < 0.05, **, P < 0.01 VS INS-1 cells at the same time point. Image collected & cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/21843373), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Western Blot: IRE1 alpha [p Ser724] Antibody - BSA Free [NB100-2323] - cCK-18 is formed following activation of the UPR. A. Immunoblots for phospho-IRE1 (p-IRE1), total IRE1 (IRE1), & cleaved cytokeratin 18 (cCK-18) showing time-dependent increase of cCK-18 in A549 cells exposed to 0.5 μM of thapsigargin (TG, +) for various lengths of time. Immunoblots showing an increase in total & phospho-IRE1 confirm thapsigargin activates the UPR in A549 cells compared to vehicle controls (−). B. Immunoblots for cCK-18 showing time-dependent appearance of cCK-18 in annexin V– or V+ A549 cells exposed to 0.5 μM of thapsigargin for various lengths of time. Image collected & cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/23167970), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Western Blot: IRE1 alpha [p Ser724] Antibody - BSA Free [NB100-2323] - Protein expression of downstream markers of ER stress in islets from lean, obese & high-fat-diet-fed fZDF rats. Protein lysates from islets isolated from three age-matched fZDF rats (obese), HF-fZDF (HFD) rats & their heterozygous lean littermates (lean) were separated by SDS-PAGE & analysed by western blotting. As controls, lysates from the islets isolated from Wistar rats or MIN6 cells treated with 1 μM thapsigargin for 2 h or sorbitol for 1 h were run alongside. Proteins were detected using antisera against (a) Calreticulin, HYOU1, GRP78, p-IRE1 alpha , p-eIF2 alpha & CHOP & as protein loading control rpS6 & (b) p-JNK & total JNK1/2 as loading control. Western blots were quantified using Image-J software. Image collected & cropped by CiteAb from the following publication (//www.nature.com/articles/nutd201335), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Western Blot: IRE1 alpha [p Ser724] Antibody - BSA Free [NB100-2323] - CETP inhibition reduces endoplasmic reticulum stress. HAECs transfected with CETP or control scrambled siRNA. (A) Western blot analysis of PERK (n = 3, * p < 0.01) & qPCR analysis of ATF6 mRNA. (B) Phosphorylated & total IRE (n = 3, ns). (C) Representative microscopic images of HAECs stained with GADD153, n = 5, & (D) Grp78/BIP, & DAPI. Scale bar, 10 μm. Mean ± SEM, n = 5, * p < 0.05. HAECs, human aortic endothelial cells. CETP, cholesteryl ester transfer protein. NS, non-silenced. siCETP, silenced CETP. PERK, protein kinase RNA-like ER kinase. ATF6, Activating transcription factor 6. IRE, inhibitor resistant esterase. BIP, binding immunoglobulin protein. GADD153, growth arrest- & DNA damage-inducible gene 153. Image collected & cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/33430172), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Western Blot: IRE1 alpha [p Ser724] Antibody - BSA Free [NB100-2323] - Activation of UPR signaling pathways after UIRI. a & b The expression of p-PERK & t-PERK in kidneys of UIRI mice were evaluated with western blot analysis & quantified. c UIRI induces the activation of ATF6 as demonstrated by enhanced expression of cleaved ATF6 (cATF6). GAPDH was used as an internal control. d Fold-change expression of cATF6 in kidneys of UIRI mouse as compared with that of sham group mouse. e & f The expression of p-IRE1 & t-IRE1 in mice kidneys were evaluated with western blotting & quantified. Data are expressed as means ± SEM, n = 3 ~ 6 in each group. *P < 0.05, **P < 0.01, & ***P < 0.001, as compared with sham group Image collected & cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/35765067), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Western Blot: IRE1 alpha [p Ser724] Antibody - BSA Free [NB100-2323] - Apoptosis mediated by Arl6ip5 interference is regulated by Chop. (a) Immunoblotting was used to detect the protein level for p-IRE1 alpha , IRE1, Chop, Arl6ip5 & beta -actin in the UAMS-32 cell with NC-siRNA or Arl6ip5-siRNA treatment for 72 h. Representative results were shown from three independent experiments. (b–e) UAMS-32 cells first received NC-siRNA or Chop-siRNA for 24 h, then the medium was changed & further received NC-siRNA or Arl6ip5-siRNA for 72 h. Q-PCR was used to analyze the mRNA levels of Chop (b), GADD34 (c) & Trib3 (d). The apoptotic cells were stained with Annexin-V & the proportion were calculated (e). n=4. In all panels, error bars represent the mean±S.E.M. **P<0.01, *P<0.05 based on ANOVA Image collected & cropped by CiteAb from the following publication (//www.nature.com/articles/cddis2014427), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Western Blot: IRE1 alpha [p Ser724] Antibody - BSA Free [NB100-2323] - Downregulation of gamma -taxilin & alpha NAC, & ER stress responses in mouse brain slice cultured under hypoxic conditions. (a) Immunohistochemistry shows downregulation of gamma -taxilin & alpha NAC expression in brain slices cultured for 48 h under hypoxic conditions. Scale bar, 20 μm. (b) Western blot shows downregulation of gamma -taxilin & alpha NAC, phosphorylation of PERK & IRE1 alpha & induction of CHOP in mouse brain slices cultured for 48 h under normoxic (−) or hypoxic conditions (+) Image collected & cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/25880086), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Western Blot: IRE1 alpha [p Ser724] Antibody - BSA Free [NB100-2323] - Differential ER stress response pathways initiated by gamma -taxilin or alpha NAC depletion. Proteins involved in UPR sensor (PERK, IRE1 alpha ), eIF2 alpha , JNK, Bcl-2, & Bcl-2-related protein (Puma, Bim, Bak, & Bax) signaling pathways were analyzed by Western blotting of HeLa S3 cells that were depleted of gamma -taxilin or alpha NAC by RNA intereference for 72 & 96 h. Upper panels, taxilin & NAC proteins; middle panels, UPR proteins; lower panels; apoptotic proteins; & bottom panel, beta -actin Image collected & cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/25880086), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Western Blot: IRE1 alpha [p Ser724] Antibody - BSA Free [NB100-2323] - The UPR is activated in type II AECs isolated from IPF lungs. Phosphorylated IRE-1 alpha (panel A) & spliced XBP-1 (panel B) were present in increased amounts in AECs from 3 different IPF lungs, but not in the 3 control subjects (* P < 0.05, **P = 0.0495 by Wilcoxon rank sum test). # indicates amplicon of unspliced XBP1 digested with Pst1. Image collected & cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/23167970), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Western Blot: IRE1 alpha [p Ser724] Antibody - BSA Free [NB100-2323] - ER stress is induced by OGR1 via IRE1 alpha /JNK signalling. (A) Caco-2 cells were subjected to different pH medium, with or without an OGR1 inhibitor (10 µM), following 4–6 h in pH 7.6 serum free medium. After 24 h pH shift, total protein was isolated & Western blot performed. Results are representative of two independent experiments. (B) Caco-2 cells were subjected to different pH medium After 24 h pH shift, total protein was isolated & Western blot performed. Results are representative of two independent experiments. (C) Caco-2 cells were subjected to different pH medium with or without a JNK inhibitor (10 µM) following 4–6 h in pH 7.6 serum free medium. After 24 h pH shift, total protein was isolated & Western blot performed. Results are representative of two independent experiments. (D) Caco-2 cells were starved & subjected to an acidic pH with or without a JNK inhibitor as described in (C). After 24 h pH shift, total RNA was isolated & mRNA expression was investigated by qPCR. Statistical analysis was performed using one-way ANOVA followed by Tukey’s post-test. Data are presented as means ± SE of three independent experiments (***p < 0.001). (E) Caco-2 cells were starved & subjected to different pH medium following 4–6 h in pH 7.6 serum free medium. After 24 h pH shift, total protein was isolated & co-IP using IRE1 alpha antibody & JNK antibody was performed, followed by immunoblotting. Results are representative of two independent experiments. pH conditions: High pH 7.5–7.8; Normal pH 7.2–7.4; Low pH 6.6–6.8. Image collected & cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/31996710), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

$Western Blot: IRE1 alpha [p Ser724] Antibody - BSA Free [NB100-2323] - Downregulation of gamma -taxilin & alpha NAC & ER stress responses in hypoxic cells. (a) Phase-contrast micrographs of SK-N-SH cells cultures in hypoxic conditions for 0–48 h. Floating cells were evident by 37 h after the beginning of hypoxic treatment. (b) FACS (fluorescence-activated cell sorting) analysis of apoptosis in hypoxic SK-N-SH cells. Bars in the FACS profiles (left panel) indicate the fraction locations of annexin-positive cells. Bar graph indicates the relative numbers of annexin-positive cells (right panel). Bar graph data are shown as means±S.D. (n=3). *Significantly different from controls (0 h) (P<0.001, Tukey–Kramer test). (c) DAPI (4',6-diamidino-2-phenylindole) staining shows fragmented nuclei of apoptotic SK-N-SH cells after hypoxic treatment. Scale bar, 10 μm. (d) Downregulation of gamma -taxilin & alpha NAC & induction of ER stress responses in hypoxic SK-N-SH cells. Western blot analysis was performed 0 to 48 h after hypoxic treatment of cells. Upper panels, taxilin & NAC proteins; middle panels, UPR proteins; lower panels, apoptotic proteins; & bottom panels, cleaved caspase-9 & beta -actin proteins. (e) MG-132 treatment restore the gamma -taxilin & alpha NAC protein level in hypoxic (16 h) HeLa S3 cells. MG-132 (−), DMSO; MG-132 (+), 20 μM. (f) Caspase inhibition does not affect the hypoxia-induced downregulation of gamma -taxilin & alpha NAC in HeLa S3 cells. (g) Colocalization of gamma -taxilin & alpha NAC in normoxic (0 h) & hypoxic (8 h) HeLa S3 cells. Note that the colocalization fraction increases with the appearance of apoptotic phenotypes. Scale bars, 10 μm Image collected & cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/25880086), licensed under a CC-BY license. Not internally tested by Novus Biologicals.$

$Western Blot: IRE1 alpha [p Ser724] Antibody - BSA Free [NB100-2323] - gamma -Taxilin ablation causes ER stress responses & apoptosis in normoxic cells. (a) Knockdown of gamma -taxilin expression by small interfering RNA (siRNA) in HeLa S3 cells. Two different siRNA constructs are equally effective. HeLa S3 cells were treated with solvent alone (Mock), control siRNA (Co), or gamma -taxilin siRNA ( gamma -tax-1 or -2) for 96 h. (b) Induction of apoptosis by gamma -taxilin ablation in HeLa S3 cells. gamma -Taxilin ablation causes apoptosis in HeLa S3 cells, but Mock or Co treatment did not. Bar graph shows fractions of annexin-positive cells (means±S.D., n=3). *Significantly different from Mock- or Co treatment (P <0.001, Tukey–Kramer test). (c) Confocal microscopy demonstrates coincidence of gamma -taxilin depletion & apoptotic nuclei in HeLa S3 cells treated with gamma -taxilin siRNA. Scale bar, 10 μm. (d) gamma -Taxilin depletion triggers ER stress responses in HeLa S3 cells. Upper panels, taxilin & NAC proteins; middle panels, UPR proteins; & lower panel, beta -actin. (e) gamma -Taxilin ablation induces accumulation of ubiquitinated proteins in HeLa S3 cells. Cell lysates were analyzed on 7.5% SDS-PAGE, followed by immunoblotting with antibodies specific for anti-mono- & polyubiquitinated conjugates (upper panel) & beta -actin (lower panel) Image collected & cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/25880086), licensed under a CC-BY license. Not internally tested by Novus Biologicals.$

$Western Blot: IRE1 alpha [p Ser724] Antibody - BSA Free [NB100-2323] - Localization of the WT & mutant Wrn proteins in different subcellular fractions.(A) Example of western blots showing the presence of the Wrn WT protein in the nuclear fraction & the presence of the Wrn delta hel mutant protein mainly in the cytosolic fraction. Fractionations were performed on WT, Wrn delta hel/ delta hel, & Wrn-/- MEFs. Topoisomerase I & beta -tubulin are nuclear & cytoplasmic markers, respectively. As expected the molecular weight of the Wrn delta hel mutant protein was lower than the Wrn WT protein. No band was detected in Wrn-/- MEFs fractions with the anti-Wrn polyclonal antibody. (B) Example of western blots showing only the presence of the Wrn delta hel mutant protein in total ER & the peroxisomal fractions. Fractionations were performed on WT, Wrn delta hel/ delta hel, & Wrn-/- liver tissues. Catalase & calreticulin are used as peroxisomal & ER specific markers. This experiment was repeated three times. (C) Protein levels of GRP78, phosphorylated IRE alpha , & beta -actin (top panels) & of total IRE alpha , & beta -actin (bottom panels) in the spleen of three animals of each genotype. (D) Ratio of GRP78 signal over beta -actin signal from western blots. (E) Ratio of IRE alpha over beta -actin signal from western blots. (F) Ratio of phosphorylated IRE alpha signal over beta -actin signal from western blots. Experiments were performed in triplicates. Bars in all histograms represent SEM. Tukey post ANOVA test P-values are shown (*P < 0.05 & **P < 0.01). Image collected & cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/26447695), licensed under a CC-BY license. Not internally tested by Novus Biologicals.$

Western Blot: IRE1 alpha [p Ser724] Antibody - BSA Free [NB100-2323] - IER3IP1 suppression decreases the UPR activation(A) mRNA levels of IRE1 alpha , Perk & Atf6 in IER3IP1 KD cells. 4 days after infection with IER3IP1 shRNA lentivirus, mRNA levels of IRE1 alpha , Perk & Atf6 in IER3IP1 KD cells were determined by qRT-PCR. *P<0.05, **P<0.01 compared to control group. Values are mean ± SEM. (B) Effect of IER3IP1 suppression on the IRE1 alpha arm of the UPR. 4 days after IER3IP1 KD in MIN6 cells, phosphorylation of IRE1 alpha , Bip, sXBP-1 & uXBP-were determined by Western blot. The loaded proteins in the two “- or +” lines were the same but from the different plates. (C) mRNA levels of downstream targets of sXBP-1 in IER3IP1 KD cells. 4 days after IER3IP1 KD in MIN6 cells, mRNA levels of downstream targets of sXBP-1, Erdj4, p58IPK, EDEM & Sec61a, were determined by qRT-PCR. Values are mean ± SEM. (D) Effect of IER3IP1 suppression on the Perk arm of the UPR. 4 days after IER3IP1 KD in MIN6 cells, phosphorylation of Perk & eIF2a, & ATF4 were determined by Western blot. The loaded proteins in the two “- or +” lines were the same but from the different plates. (E) IER3IP1 KD decreases UPR activation induced by ER stress in MIN6. 4 days after IER3IP1 KD, MIN6 cells were treated with 10 μg/ml tunicamycin (TC) or 1 μM thapsigargin (TG) for 6 hours. Then the expression levels of Chop, sXBP-1, uXBP-1 & IER3IP1 were determined by Western blot. Image collected & cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/28915629), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Western Blot: IRE1 alpha [p Ser724] Antibody - BSA Free [NB100-2323] - ATG5 & ATG7 influenced on autophagy, apoptosis & cell cycle through PERK/Nrf2 signaling. a The ER stress proteins were analysed by western blotting in Ad-GFP, Ad-ATG5 + Ad-ATG7,Ad-ATG5 + Ad-ATG7 + siPERK,Ad-ATG5 + Ad-ATG7 + siNrf2 & Ad-ATG5+ Ad-ATG7 + siPERK+siNrf2 induced chondrocytes. b The levels of ER stress proteins were normalized to beta -actin. c Determination of autophagy & apoptosis proteins expression by western blotting in Ad-GFP, Ad-ATG5 + Ad-ATG7, Ad-ATG5 + Ad-ATG7 + siPERK,Ad-ATG5 + Ad-ATG7 + siNrf2 & Ad-ATG5+ Ad-ATG7 + siPERK+ siNrf2 induced chondrocytes. dThe levels of related proteins were normalized to beta -actin. e FCM analysis was used to calculate the percentage of apoptotic cells at the time point of 24 h. The apoptosis rate were increased when combined treatment with silencing of PERK or Nrf2. Experiments were repeated 3 times, Representative images are shown. f Analysis of cell apoptosis. Data come from 3 independent experiments. g FCM analysis indicated that the S phase percentage were decreased compared to that of the control groups when combine infected with silencing of PERK or Nrf2 in C28I2 cells. Experiments were repeated 3 times, Representative images are shown. h Percentage of cells at each phase in different groups. *P < 0.05, **P < 0.01 compared with the controls. Values are means ± SD n = 3). (1:Ad-GFP, 2:Ad-ATG5 + Ad-ATG7, 3:Ad-ATG5 + Ad-ATG7 + siPERK, 4:Ad-ATG5 + Ad-ATG7 + siNrf2, 5:Ad-ATG5 + Ad-ATG7 + siPERK+ siNrf2) Image collected & cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/31060556), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Western Blot: IRE1 alpha [p Ser724] Antibody - BSA Free [NB100-2323] - Thapsigargin treatment induces calpain activation & autophagy. (A) Control & shCAPNS1 cells were treated with 100 nM thapsigargin for 10, 20 & 30 min & the lysates subjected to western blot analysis to quantify the precursor & active form of CAPN1. The ratio between active CAPN1 & tubulin is reported below each lane. (B) Time course measurement of intracellular calcium concentration. The plot indicates the ratio of mean Indo Violet/Indo Blue emission values of each cell population at individual time points (minutes). The ratio corresponds to the relative calcium concentration of control & shCAPNS1 U2OS cells before & after addition of thapsigargin (100 nm final). Moving average was used as smoothing method. (C) shCAPNS1 cells were treated with 100 nM thapsigargin for 30, 60 & 120 min & the lysates subjected to western blot analysis to detect LC3, p62, pIRE, CAPNS1 & tubulin. (D) Levels of p62 & LC3 normalized to tubulin levels. Image collected & cropped by CiteAb from the following publication (//journals.biologists.com/bio/article/doi/10.1242/bio.022806/256614/Calpain-mobilizes-Atg9-Bif-1-vesicles-from-Golgi), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Western Blot: IRE1 alpha [p Ser724] Antibody - BSA Free [NB100-2323] - Abnormal Paneth cells show ER stress.(A, B) Representative transmission electron microscopy images of Paneth cells at the base of ileal crypts in (A) ICR & (B) SAMP1/YitFc mice. Scale bars indicate 2 μm. (C, D) Quantitative analysis of (C) granule number & (D) ER lumen diameter in Paneth cells (n = 3/each week for SAMP1/YitFc mice). For the measurements, three Paneth cells were randomly selected from each mouse. (E) SDS–PAGE Western blot analysis of ER stress markers, pIRE1 alpha , ATF4, cleaved-ATF6, & GRP78 in ileal crypts (n = 4/each group). Total-IRE1 alpha & HPRT1 was used as loading control. (F) Relative expression level of ER stress markers calculated from the band intensity. Error bars represent mean ± SEM. (C, D, F) Statistical significance was evaluated by t test in (C, D), & one-way ANOVA followed by Tukey’s post hoc test in (F). P < 0.05 was considered statistically significant. *P < 0.05, †P < 0.01, §P < 0.001. E, ER; G, granules; N, nucleus; n.s., not significant. Image collected & cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/32345659), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Western Blot: IRE1 alpha [p Ser724] Antibody - BSA Free [NB100-2323] - Hypoxia-induced downregulation of gamma -taxilin & alpha NAC & the subsequent ER responses are GSK-3 beta -dependent. (a) GSK-3 beta activation in hypoxia. Western blot analysis shows downregulation of phosphorylated (Ser 9) GSK-3 beta (phospho-GSK-3 beta ) in hypoxic (0–48 h) SK-N-SH & hypoxic (0–24 h) HeLa S3 cells. (b) Inhibition of GSK-3 beta activation by lithium chloride (LiCl, 100 mM) or CHIR-99021 (CHIR, 15 or 30 μM) maintained gamma -taxilin & alpha NAC protein levels in hypoxic SK-N-SH & HeLa S3 cells. (c) GSK-3 beta inhibition suppresses the expression of ER stress response proteins that are induced in hypoxic SK-N-SH cells. (d) GSK-3 beta RNA interference almost completely blocked the protein expression & restored the expression of gamma -taxilin & alpha NAC proteins in hypoxic HeLa S3 cells Image collected & cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/25880086), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Reactivity:

Hu, Mu, Rt, Po, Dr, Gt, Ma, Pm, Pm, Rb, SyHa

Species Glossary

Reactivity: Hu, Mu, Rt, Po, Dr, Gt, Ma, Pm, Pm, Rb, SyHa

Applications:

, , , , , , , , ,

Applications: , , , , , , , , ,

Host:

Rabbit Polyclonal

Host: Rabbit Polyclonal

Sizes:

Sample Size Available

Sizes: Sample Size Available

Conjugate:

Unconjugated

Available Conjugates:

Validated by:

Validated by:

Conjugate	Catalog #	Availability	Size	Price
Alexa Fluor 350	NB100-2323AF350
Alexa Fluor 405	NB100-2323AF405
Alexa Fluor 488	NB100-2323AF488
Alexa Fluor 532	NB100-2323AF532
Alexa Fluor 594	NB100-2323AF594
Alexa Fluor 647	NB100-2323AF647
Alexa Fluor 700	NB100-2323AF700
Alexa Fluor 750	NB100-2323AF750
Allophycocyanin	NB100-2323APC
Biotin	NB100-2323B
CoraFluor 1	NB100-2323CL1
DyLight 350	NB100-2323UV
DyLight 405	NB100-2323V
DyLight 488	NB100-2323G
DyLight 550	NB100-2323R
DyLight 594	NB100-2323DL594
DyLight 650	NB100-2323C
DyLight 680	NB100-2323FR
DyLight 755	NB100-2323IR
FITC	NB100-2323F
HRP	NB100-2323H
Janelia Fluor 525	NB100-2323JF525
Janelia Fluor 549	NB100-2323JF549
Janelia Fluor 646	NB100-2323JF646
Janelia Fluor 669	NB100-2323JF669
PE	NB100-2323PE
PerCP	NB100-2323PCP
mFluor Violet 450 SE	NB100-2323MFV450
mFluor Violet 500 SE	NB100-2323MFV500
mFluor Violet 610 SE	NB100-2323MFV610

Available Formulations

Formulation	Catalog #	Availability	Price
BSA Free	NB100-2323SS

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NB400-132

ABCG1 Antibody - BSA Free

(2 Reviews)

(186 Publications)

0.1 ml

NB400-132

Flow (Intracellular): ABCG1 Antibody - BSA Free [NB400-132] - RAW 246.7 cells were either untreated (A) or serum starved for 24 hours, and then treated with 1uM TO9 for 24 hours (B). An intracellular stain was performed with NB400-132 (blue) and a matched isotype control NB810-56910 (orange). Cells were fixed with 4% paraformaldehyde, following fixation, cells were permeabilized with 0.1% saponin. Cells were incubated in an antibody dilution of 5 ug/mL for 30 minutes at room temperature, followed by Goat Anti-Rabbit Dylight 550-conjugated antibody.

<b>Biological Strategies Validation. </b>Western Blot: ABCG1 Antibody - BSA Free [NB400-132] - Cells were pretreated with 5 uM F12511 or 5 uM MG132 for 30 min and then exposed to 5 or 50 uM 24S-OHC for 6 h. Whole-cell lysates were immunoblotted with antibodies specific for ABCG1 or beta-actin. Image collected and cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/31285856/) licensed under a CC-BY license.

Western Blot: ABCG1 Antibody - BSA Free [NB400-132] - Detection of ABCG1 in J774 mouse macrophages. Image provided by Dr. Angeliki Chroni of the National Centre for Scientific Research Demokritos.

Western Blot: ABCG1 Antibody - BSA Free [NB400-132] - Raw 264.7 (A), and Raw 264.7 + 10uM T09 18 hr (B) cell lysate using ABCG1 antibody at 2 ug/mL.

Western Blot: ABCG1 Antibody - BSA Free [NB400-132] - Detection of ABCG1 in mouse peritoneal macrophages. Lane 1: untreated mouse peritoneal macrophages, Lane 2: 22-(R)-hydrocholesterol treated macrophages, Lane 3: T0901713 treated macrophages, Lane 4: T091713 treated macrophages.

Western Blot: ABCG1 Antibody - BSA Free [NB400-132] - SAA has little impact on the impairment in biliary and fecal excretion of macrophage-derived 3H-cholesterol during endotoxemia. WT and SAAKO mice were injected subcutaneously with PBS or 0.8 ug/g LPS as indicated, followed 4 hr later by intraperitoneal injection of 3H-cholesterol-labeled J774 macrophages. ABCG1 in liver lysates (40 ug protein) was identified by immunoblotting and quantified by densitometry. Results from each of the 3 experiments (n = 4-5 per group per experiment) were expressed relative to PBS-injected WT mice after normalization to beta-actin. A representative western blot is shown. Image collected and cropped by CiteAb from the following publication (//www.hindawi.com/journals/jl/2013/283486/), licensed under a CC-BY license.

miR-33 deficiency improved cholesterol efflux in macrophages. A, Quantitative real-time PCR analysis of Abca1 & Abcg1 in macrophages from miR-33+/+Apoe−/− & miR-33−/−Apoe−/− mice. Values from miR-33+/+Apoe−/− were set at 100%. Values are mean±SE (n=7 each); ***P<0.001. B, Western blotting analysis of ABCA1 & ABCG1 in thioglycollate-elicited peritoneal macrophages from miR-33+/+Apoe−/− & miR-33−/−Apoe−/− mice. GAPDH was used as a loading control. C, Cholesterol efflux from thioglycollate-elicited peritoneal macrophages in the presence or absence of apoA-I (5 or 10 μg/mL). Values are mean±SE (n=6 each); **P<0.01. D, Cholesterol efflux from thioglycollate-elicited peritoneal macrophages in the presence or absence of HDL-C (50 or 100 μg/mL). Values are mean±SE (n=6 each); **P<0.01. Image collected & cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/23316322), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

6‐Dihydroparadol increases A) ABCA1 & B) ABCG1, but not C) SR‐BI protein levels in cholesterol‐loaded THP‐1‐derived macrophages. THP‐1 cells were differentiated as described in Figure 2, & then loaded with unlabeled cholesterol for 24 h. Cells were treated with increasing concentrations of 6‐dihydroparadol (1–30 μm) for another 24 h. The protein levels of ABCA1, ABCG1, & SR‐B1 were detected by Western blot analysis. The control was treated with solvent vehicle (0.1% DMSO). As a positive control, TO901317 (5 μm, 24 h) was used. The bar graphs represent mean ± SD from three independent experiments. *p < 0.05, **p < 0.01, & ***p < 0.001 versus control (determined by Student's t‐test or ANOVA with Bonferroni's post hoc test). Image collected & cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/29802792), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

(A) Chemical structure, (B) cytotoxicity of alpha -asarone, (C) enhancement of cholesterol efflux by alpha -asarone, (D & E) upregulation of ABCA1 & ABCG1 by alpha -asarone & beta -asarone, & (F) elevation of retinoid X receptor (RXR) alpha transcription. J774A.1 murine macrophages were exposed to 50 μg/ml oxidized low-density lipoprotein (LDL) & treated with 1–10 μM purple Perilla frutescens extracts (PPE)-alpha -asarone & 5–10 μM beta -asarone. (B) MTT assay was performed for the measurement of alpha -asarone toxicity. Graph data represent 1 of 4 independent experiments with multiple estimations. Values are expressed as the percentage cell survival relative to the untreated control cells (cell viability, 100%). (C) Cholesterol efflux was expressed as the percentage fluorescence in the medium relative to total fluorescence. (D & E) For the measurement of ABCA1 & ABCG1 expression, total cell lysates were subjected to western blot analysis with a primary antibody against ABCG1 or ABCG1. beta -actin was used as an internal control. Bar graphs (means ± SEM, n=3) represent quantitative densitometric results of the upper bands. Bar graphs denoted without a common letter indicate significant difference, P<0.05. (F) RXR alpha mRNA expression was measured by RT-PCR. GAPDH was used as a housekeeping gene for the co-amplification with RXR alpha . Image collected & cropped by CiteAb from the following publication (//www.spandidos-publications.com/10.3892/ijmm.2015.2101), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

6‐Dihydroparadol increases A) ABCA1 & B) ABCG1 protein stability. THP‐1 cells were differentiated as described in Figure 2. Then cells were loaded with unlabeled cholesterol & treated with 6‐dihydroparadol (10 μm), or solvent vehicle (0.1% DMSO, control) for 24 h. Cells were lysed at different time points (0, 1, 2, 3, 4, & 6 h) after treatment with the protein synthesis inhibitor cycloheximide (CHX, 100 μm). The protein levels of both ABCA1 & ABCG1 were detected by Western blot analysis. The data points represent mean ± SD from three independent experiments. *p < 0.05 & **p < 0.01 versus control at the same time point (determined by Student's t‐test). Image collected & cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/29802792), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

(A) Upregulation of ABCA1 & ABCG1 & (B) enhancement of cholesterol efflux by purple Perilla frutescens extracts (PPE) in 50 μg/ml Cu2+-oxidized low-density lipoproteins (LDL)-exposed J774A.1 murine macrophages. (A) For the measurement of ABCA1 & ABCG1 expression, total cell lysates were subjected to western blot analysis with a primary antibody against ABCA1 or ABCG1. beta -actin was used as an internal control. Bar graphs (means ± SEM, n=3) represent quantitative densitometric results of the upper bands. (B) Cholesterol efflux was expressed as the percentage of fluorescence in the medium relative to the total fluorescence. Bar graphs denoted without a common letter indicate significant difference, P<0.05. Image collected & cropped by CiteAb from the following publication (//www.spandidos-publications.com/10.3892/ijmm.2015.2101), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Western Blot: ABCG1 Antibody - BSA Free [NB400-132] - 6‐Dihydroparadol increases A) ABCA1 & B) ABCG1 protein stability. THP‐1 cells were differentiated as described in Figure 2. Then cells were loaded with unlabeled cholesterol & treated with 6‐dihydroparadol (10 μm), or solvent vehicle (0.1% DMSO, control) for 24 h. Cells were lysed at different time points (0, 1, 2, 3, 4, & 6 h) after treatment with the protein synthesis inhibitor cycloheximide (CHX, 100 μm). The protein levels of both ABCA1 & ABCG1 were detected by Western blot analysis. The data points represent mean ± SD from three independent experiments. *p < 0.05 & **p < 0.01 versus control at the same time point (determined by Student's t‐test). Image collected & cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/29802792), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Western Blot: ABCG1 Antibody - BSA Free [NB400-132] - Evodiamine enhances apo A1-mediated ChE from THP-1 macrophages & increases ABCA1 protein level. (a) Differentiated THP-1 cells were loaded with [3H]-cholesterol together with the indicated treatments for 24 h. On the next day, the cells were washed twice with PBS & incubated with the same compounds [solvent vehicle control (Veh; ≤0.1% DMSO), evodiamine (1–20 μM), & the PPAR gamma agonist pioglitazone (10 μM) as positive control] with or without 10 µg/mL apo A1. Extracellular as well as intracellular radioactivities were quantified with scintillation counter. Differentiated THP-1-derived macrophages were treated with solvent vehicle control (Veh; ≤0.1% DMSO), evodiamine (10 μM), & the PPAR gamma agonist pioglitazone (10 μM) as positive control. After 24 h incubation, the cells were lysed & 20 μg protein was resolved via SDS-PAGE. Immunodetection was performed with antibodies against the indicated proteins, ABCA1 (b), ABCG1 (c), & SR-B1 (d), & visualized by chemiluminescence detection. All experiments were performed at least three times & data are presented as means ± S.D. vs. solvent vehicle control, *p < 0.05, **p < 0.01, ***p < 0.001, n.s. no significance (ANOVA/Bonferroni). Image collected & cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/30038271), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Reactivity:

Hu, Mu, Rt, ChHa, Ha, Pm, Rb

Species Glossary

Reactivity: Hu, Mu, Rt, ChHa, Ha, Pm, Rb

Applications:

, , , , , , ,

Applications: , , , , , , ,

Host:

Rabbit Polyclonal

Host: Rabbit Polyclonal

Sizes:

Sample Size Available

Sizes: Sample Size Available

Conjugate:

Unconjugated

Available Conjugates:

Validated by:

Validated by:

Conjugate	Catalog #	Availability	Size	Price
Alexa Fluor 350	NB400-132AF350
Alexa Fluor 405	NB400-132AF405
Alexa Fluor 488	NB400-132AF488
Alexa Fluor 532	NB400-132AF532
Alexa Fluor 594	NB400-132AF594
Alexa Fluor 647	NB400-132AF647
Alexa Fluor 700	NB400-132AF700
Alexa Fluor 750	NB400-132AF750
Allophycocyanin	NB400-132APC
Allophycocyanin/Cy7	NB400-132APCCY7
Biotin	NB400-132B
CoraFluor 1	NB400-132CL1
DyLight 350	NB400-132UV
DyLight 405	NB400-132V
DyLight 488	NB400-132G
DyLight 550	NB400-132R
DyLight 594	NB400-132DL594
DyLight 650	NB400-132C
DyLight 680	NB400-132FR
DyLight 755	NB400-132IR
FITC	NB400-132F
HRP	NB400-132H
Janelia Fluor 525	NB400-132JF525
Janelia Fluor 549	NB400-132JF549
Janelia Fluor 646	NB400-132JF646
Janelia Fluor 669	NB400-132JF669
PE	NB400-132PE
PE/Atto594	NB400-132PEATT594
PE/Cy5.5	NB400-132PECY55
PE/Cy7	NB400-132PECY7
PerCP	NB400-132PCP
mFluor Violet 450 SE	NB400-132MFV450
mFluor Violet 500 SE	NB400-132MFV500
mFluor Violet 610 SE	NB400-132MFV610

Available Formulations

Formulation	Catalog #	Availability	Price
BSA Free	NB400-132SS

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NB300-605

iNOS Antibody - BSA Free

(3 Reviews)

(143 Publications)

200uL

NB300-605

Immunohistochemistry-Paraffin: iNOS Antibody [NB300-605] - Immunohistochemistry was performed on normal deparaffinized human Heart tissue.

Immunocytochemistry/Immunofluorescence: iNOS Antibody [NB300-605] - Analysis of iNOS in A549 Cells. Cells were grown on chamber slides and fixed with formaldehyde prior to staining. Cells were probed without (control) or with a iNOS polyclonal antibody at a dilution of 1:20 overnight at 4C, washed with PBS and incubated with a DyLight 488 conjugated secondary antibody. iNOS staining (green), F-Actin staining with Phalloidin (red) and nuclei with DAPI (blue) is shown.

<b>Biological Strategies Validation. </b>Western Blot: iNOS Antibody [NB300-605] - iNOS in stimulated astrocytes. Western blot image submitted by a verified customer review.

<b>Biological Strategies Validation. </b>Western Blot: iNOS Antibody [NB300-605] - LCA-induced oxidative stress in 4T1 breast cancer cells. The 4T1 cells were treated with LCA for 48 h, then the indicated measurements were performed. The level of iNOS protein was detected by western blotting (n = 3). Image collected and cropped by CiteAb from the following publication (//www.mdpi.com/2072-6694/11/9/1255), licensed under a CC-BY license.

Immunocytochemistry/Immunofluorescence: iNOS Antibody [NB300-605] - Analysis of iNOS in NIH-3T3 Cells. Cells were grown on chamber slides and fixed with formaldehyde prior to staining. Cells were probed without (control) or with a iNOS polyclonal antibody at a dilution of 1:20 overnight at 4C, washed with PBS and incubated with a DyLight 488 conjugated secondary antibody. iNOS staining (green), F-Actin staining with Phalloidin (red) and nuclei with DAPI (blue) is shown.

Western Blot: iNOS Antibody - BSA Free [NB300-605] - Stimulation of IMA 2.1 cells had no effect on relative survival after viral infection. IMA 2.1 cells were stimulated with LPS (10 µg/ml), IFN-gamma , (10 ng/ml) LPS + IFN-gamma , IL-4 (10 ng/ml), FGF (5 ng/ml) or FGF + LPS for 24 h in medium with 2% FBS. Polarization of cells was analyzed by Griess assay (a), Western blot (b) & FACS analysis by detection of MHCII+ cells (c). d MTT assay was performed to detect the relative percentage of VACV-mediated cell death in the presence of stimulating factors. e Viral replication was analyzed by standard plaque assay in the presence of stimulating factors. All experiments were performed in triplicate. Image collected & cropped by CiteAb from the following publication (//www.translational-medicine.com/content/13/1/216), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Immunocytochemistry/ Immunofluorescence: iNOS Antibody - BSA Free [NB300-605] - Nfix is mainly expressed by anti-inflammatory MPs. (a) Percentage of F4/80+ MPs positive for Nfix in Tibialis Anterior muscles (TA) of WT mice injected by CTX at D2, D4 & D7, post-injury. Immunostaining for F4/80 (green), Nfix (red) & DAPI (blue) at D4 & D7 after CTX injection; (b) Percentage of Ly6C+ & Ly6C- sorted MPs positive for Nfix in TA muscles of WT mice injected by CTX at D2, D4 & D7 post-injury; (c) Percentage of Nfix+ MPs after M1 & M2c polarization (with IFN gamma & IL10, respectively). * p < 0.05; *** p < 0.001; for (b) * p < 0.05 Ly6C+ vs. Ly6C+ at D4 & D7; # p < 0.05 Ly6C− D7 vs. D2. Results are means ± SEM of at least three independent experiments. Scale bar = 50 μm. Image collected & cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/32183151), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Western Blot: iNOS Antibody - BSA Free [NB300-605] - Indolepropionic acid (IPA) induced oxidative stress, cellular energy stress, & decreased the proportions of cancer stem cells. 500,000 cells/well 4T1 cells were treated with IPA in the concentrations indicated for 24 h; then, (A) lipid peroxidation was measured by TBARS assay, & (B) 4HNE expression was assessed by Western blotting (representative figure, n = 3). In the same cells (C), the protein expression of NRF2 (at 68 kDa) & iNOS were determined by Western blotting (n = 3), while (D) the mRNA expression of catalase (cat) was determined by RT-qPCR (n = 3). (E) The expression of the indicated proteins (pACC, ACC, FOXO1, & PGC-1 beta ) were determined by Western blotting (n = 3, except for PGC-1 beta , where n = 2). (F) 100,000 cells/well 4T1 cells were treated with the indicated concentration of IPA for 24 h; then, the proportions of aldehyde dehydrogenase-positive cells were determined in Aldefluor assays using flow cytometry (n = 3). For Western blots, a typical experiment was displayed. Fold data were log2 transformed to achieve normal distribution. Statistical significance was determined using the ANOVA test followed by Dunnett’s post-hoc test, except for panel F, where Student’s t-test was used. * & *** indicate statistically significant difference between control & treated samples at p < 0.05 & p < 0.001, respectively. Image collected & cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/32854297), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Western Blot: iNOS Antibody - BSA Free [NB300-605] - NRF2 activation modulated LCA-induced oxidative stress responses in 4T1 breast cancer cells. The 4T1 cells were treated with 0.3 μm LCA & the NRF2 activator RA839 or tBHQ in the concentrations indicated for 48 h. Lipid peroxidation was determined by measuring (A) TBARS (n = 4) & (B,C) 4-HNE levels using western blotting (n = 3). (D) The 4T1 cells were treated with LCA (0.3 μm) and/or GSH & NAC (both at 5 mm) antioxidants for 48 h, then total protein concentration was determined using the sulforhodamine B assay (n = 3). For statistical analysis ANOVA test was used followed by the Dunnett post-hoc test, where all groups were compared to the LCA-treated cohort. Data are plotted as mean ± SEM. ** p < 0.01, LCA vs. LCA/NRF2-activator-treated groups (GSH, reduced glutathione; LCA, lithocholic acid; NAC, N-acetylcysteine; TBARS, thiobarbituric acid reactive substances; 4HNE, 4-hydroxynonenal). Image collected & cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/31461945), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Western Blot: iNOS Antibody - BSA Free [NB300-605] - Impaired amount of virus progeny after stimulation of BV-2 cells with IFN-gamma or IFN-gamma & LPS. BV-2 cells were stimulated with LPS (10 µg/ml), IFN-gamma , (10 ng/ml), LPS + IFN-gamma or IL-4 (10 ng/ml) for 24 h in medium with 2% FBS. Polarization of cells was analyzed by Griess assay (a), Western blot (b) & by detection of the percentage of MHCII+ cells by FACS analysis (c). The amount of virus progeny (pfu/ml) was analyzed by standard plaque assay in the presence of stimulating factors & in normal growth medium in cells & supernatants (d). Statistical analysis was performed related to infection medium. To analyze the recovery of viral replication, normal growth medium was applied after infection of pre-stimulated cells. Standard plaque assay was performed to determine viral progeny in cells & supernatant after 24, 48, 72 & 96 hpi (e). To analyze the relative survival of the cells in the presence of stimulating factors a MTT assay was performed (f). The cellular density of stimulated cells relative to unstimulated (w/o) cells was detected via optical density measurement after 24 & 48 h of cultivation (g). Two-sided t test with unequal variances was used for statistics *p < 0.05, **p < 0.01, ***p < 0.001. Active replication was defined as virus titer above the virus titer of the infection medium (red line). All experiments were performed in triplicate & repeated in an independent experiment. Image collected & cropped by CiteAb from the following publication (//www.translational-medicine.com/content/13/1/216), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Western Blot: iNOS Antibody - BSA Free [NB300-605] - Inhibitory effect of MMPP on amyloidogenesis & STAT3 translocation in astrocytes & microglia cells. The expression of APP, BACE1 & C99 was detected by Western blotting using specific antibodies in astrocytes (a) & microglia cells (b). Each blot is representative of three experiments. The activity of beta -secretase was investigated using assay kit in astrocytes (c) & microglia cells (d). Values are presented as mean ± S.D. of the three independent experiments performed in triplicate. #p < 0.05 compared to control, *p < 0.05 compared to LPS. Iba-1, COX-2, & iNOS proteins were detected by Western blotting using specific antibodies in astrocytes (e) & microglia cells (f). NO level was measured in astrocytes (g) & microglia cells (h). Activation of STAT3 was investigated using EMSA in astrocytes (i) microglial cells (j) were determined & the expression of STAT3 & phopho-STAT3 was also detected by Western blotting using specific antibodies (k), (l). For the cropped images, samples were run in the same gels under same experimental conditions & processed in parallel. Each band is representative for three experiments Image collected & cropped by CiteAb from the following publication (//link.springer.com/10.1007/s12017-017-8469-3), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

TSA, PXD, or MGCD restore osteoimmune balance and reduce osteolytic activity. A Histological examination by H&E staining revealed differences in calvarial bone morphology between groups. Immunohistochemical staining demonstrated that treatment with TSA, PXD, or MGCD reduced osteoclast activity, as shown by decreased CTSK expression (B), suppressed M1 macrophage polarization indicated by reduced iNOS expression (D), enhanced M2 macrophage polarization indicated by increased ARG1 expression (F), and promoted osteogenesis as reflected by elevated RUNX2 expression (H). Quantification of CTSK- (C), iNOS- (E), ARG1- (G), and RUNX2- (I) positive cells. Data are presented as mean +/- SD (n = 6 per group). *P < 0.05, **P < 0.01, and ***P < 0.001. Scale bar = 100 μm Image collected and cropped by CiteAb from the following open publication (//pubmed.ncbi.nlm.nih.gov/41174647), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Reactivity:

Hu, Mu, Rt, Po

Species Glossary

Reactivity: Hu, Mu, Rt, Po

Applications:

, , , , ,

Applications: , , , , ,

Host:

Rabbit Polyclonal

Host: Rabbit Polyclonal

Sizes:

Sample Size Available

Sizes: Sample Size Available

Conjugate:

Unconjugated

Available Conjugates:

Validated by:

Validated by:

Conjugate	Catalog #	Availability	Size	Price
Alexa Fluor 405	NB300-605AF405
Alexa Fluor 488	NB300-605AF488
Alexa Fluor 647	NB300-605AF647
Alexa Fluor 700	NB300-605AF700
Biotin	NB300-605B
DyLight 350	NB300-605UV
DyLight 405	NB300-605V
DyLight 488	NB300-605G
DyLight 550	NB300-605R
DyLight 594	NB300-605DL594
DyLight 650	NB300-605C
DyLight 680	NB300-605FR
DyLight 755	NB300-605IR
FITC	NB300-605F
HRP	NB300-605H
Janelia Fluor 549	NB300-605JF549
Janelia Fluor 646	NB300-605JF646

Available Formulations

Formulation	Catalog #	Availability	Price
BSA Free	NB300-605SS

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NB110-89474

CD11b Antibody - BSA Free

(12 Reviews)

(130 Publications)

0.1 ml

NB110-89474

Western Blot: CD11b Antibody - BSA Free [NB110-89474] - Western Blot detection of CD11b in RAW 264.7 whole cell lysates using [NB110-89474].

Immunocytochemistry/Immunofluorescence: CD11b Antibody - BSA Free [NB110-89474] - Staining of mouse pancreas using [NB110-89474] at 1:400 dilution. Nuclei counterstained with 4',6-diamidino-2-phenylindole (DAPI) (blue). ICC/IF image submitted by a verified customer review.

Immunohistochemistry: CD11b Antibody - BSA Free [NB110-89474] - Glibenclamide and Abcc8-/- suppress immune cell infiltration in EAE. White matter of lumbar spinal cord sections from WT control (a), untreated pid-30 WT/EAE (b), glibenclamide-treated pid-30 WT/EAE (c), and pid-30 Abcc8-/-/EAE (d) mice, stained with H&E or immunolabeled for CD45 (leucocyte), CD3 (T cells), CD20 (B cells), or CD11b (macrophage/microglia), as indicated; original magnification, x200 (H&E) or x400 (all immunolabelings). eleft panel: percent of quadrants with inflammatory cells on H&E; four mice/group. efour right panels: Quantification of CD-45-, CD3-, CD20-, and CD11b-expressing cells in white matter; four mice/group; ##P < 0.01 with respect to WT control; **P < 0.01, and ***P < 0.001 with respect to WT/EAE; scale bars, 100 um Image collected and cropped by CiteAb from the following publication (//www.jneuroinflammation.com/content/12/1/210) licensed under a CC-BY license.

Flow (Cell Surface): CD11b Antibody - BSA Free [NB110-89474] - Surface staining of CD11b in CT26 colorectal carcinoma tumor model. Using Alexa Fluor 405 conjugated version of the antibody (NB110-89474AF405). Image from verified customer review.

Immunocytochemistry/Immunofluorescence: CD11b Antibody - BSA Free [NB110-89474] - CD11b Antibody [NB110-89474] - CD11b antibody [NB110-89474] was tested in Raw264.7 cells with DyLight 488 (green). Nuclei and alpha-tubulin were counterstained with 4',6-diamidino-2-phenylindole (DAPI) (blue) and DyLight 550 (red).

Immunohistochemistry: CD11b Antibody - BSA Free [NB110-89474] - Population of CD11b + myeloid progenitor cells differentiate into SMA + stromal cells within tumors and in vitro. Representative image of CD11b + SMA + double positive cells within tumor stroma. Image collected and cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/32731354/) licensed under a CC-BY license.

Immunohistochemistry: CD11b Antibody - BSA Free [NB110-89474] - Immunohistochemical analysis of CD11b in human renal cancer with [NB110-89474] using 3,3'-Diaminobenzidine (DAB) with hematoxylin counterstain.

Immunohistochemistry-Frozen: CD11b Antibody - BSA Free [NB110-89474] - Immunohistochemical analysis of frozen sections of mouse spleen using [NB110-89474]. IHC-Fr image submitted by a verified customer review.

Immunohistochemistry: CD11b Antibody - BSA Free [NB110-89474] - Representative photomicrographs of cross sections of uteri collected from wild type (WT) mice 24 h after intrauterine infusion with 100 ul of vehicle or 100 ug ultrapure LPS from E. coli O111:B4, and Tlr4-/- mice similarly infused intrauterine with vehicle or LPS. Cross sections were stained with haematoxylin and eosin, and immunostained using a CD11b antibody for granulocytes (red) and DAPI for cell nuclei (white), and images collected at 10X magnification sections (C, F, I, L; bars = 200 um). At least 4 sections per animal and at least 4 fields per section were examined. Only WT mice infused with LPS show evidence of inflammation and accumulation of granulocytes in the endometrium. Image collected and cropped by CiteAb from the following publication (//dx.plos.org/10.1371/journal.pone.0012906) licensed under a CC-BY license.

Flow (Cell Surface): CD11b Antibody - BSA Free [NB110-89474] - CD11b Antibody [NB110-89474] - A surface stain was performed on Raw264.7 cells with DyLight 550-conjugated [NB110-89474R] (blue) and a matched isotype control (orange). Cells were incubated in an antibody dilution of 10 ug/mL for 20 minutes at room temperature. Both antibodies were conjugated to DyLight 550.

Flow (Cell Surface): CD11b Antibody - BSA Free [NB110-89474] - An intracellular stain was performed on THP-1 cells with CD11b NB110-89474 (blue) and a matched isotype control NBP2-24891 (orange). Cells were incubated in an antibody dilution of 2.5 ug/mL for 30 minutes at room temperature, followed by Rabbit IgG (H+L) Cross-Adsorbed Secondary Antibody, Dylight 550 (SA5-10033, Thermo Fisher).

Simple Western: CD11b Antibody - BSA Free [NB110-89474] - Specific band for Cd11b in 1.0 mg/mL of Dentate Gyrus from Rat Brain. [NB110-89474] was used at a dilution of 1:50. This experiment was performed under reducing conditions using the 12-230 kDa separation system. Simple Western image submitted by a verified customer review.

Dual RNAscope ISH-IHC: CD11b Antibody - BSA Free [NB110-89474] - Formalin-fixed paraffin-embedded tissue sections of human lymph node were probed for CD11b mRNA (ACD RNAScope Probe, catalog #555098; Fast Red chromogen, ACD catalog # 322750). Adjacent tissue section was processed for immunohistochemistry using Rabbit Polyclonal (Novus Biologicals catalog #NB110-89474) at 1:50 dilution with 1 hour incubation at room temperature followed by incubation with anti-rabbit IgG VisUCyte HRP Polymer Antibody (Catalog # VC003) and DAB chromogen (yellow-brown). Tissue was counterstained with hematoxylin (blue). Specific staining was localized to lymphocytes.

Dual RNAscope ISH-IHC: CD11b Antibody - BSA Free [NB110-89474] - CD14 mRNA (red) and CD11b protein (green) were detected in formalin-fixed paraffin-embedded tissue sections of human malignant lymph node. ACD's Integrated Co-Detection Workflow was performed using ACD RNAScope Probe Hs-CD14 and CD11b antibody at 1:200 dilution. Tissue was stained on Leica Bond RX using RNAscope (TM) 2.5 LS Reagent Kit-RED, BOND Polymer Refine Detection (DAB) and Hematoxylin, BOND Polymer Refine Red Detection and Hematoxylin and RNA scope (TM) 2.5 LS Green Accessory Pack. Tissue was counterstained with 50% hematoxylin (blue).

CD11b staining in IMhu. Cells were stained with antibodies against the CD11b surface antigen. (A) Panel A shows positive staining for CD11b and (B) panel B shows nuclear DAPI staining. Magnitude 40×.

Western Blot: CD11b Antibody - BSA Free [NB110-89474] - Immunodensities of (a) CD11b, (b) GFAP & (c) NF-kappa B (p65) proteins with representative immunoblots in striatum from Munc18-OE (n = 5) & wild-type (n = 5) mice. Bar graphs are ratios of optical densities of our proteins of interest to beta -actin (42 kDa band), expressed as immunoreactivity in percentage of mean value of the WT group (100%). No differences were detected between groups for any of the analyzed proteins. Right panels are representative immunoblots for target proteins & beta -actin which included Munc18-OE (OE) & wild-type (WT) mice samples. The molecular masses were estimated from referenced standards. Image collected & cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/25069615), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Immunohistochemistry: CD11b Antibody - BSA Free [NB110-89474] - Comparison of Ki-67 or CD11b immunoreactivity of Aldara-treated dorsal skin samples of C57BL/6 mice using OP or MP. Nuclear proliferation marker Ki-67 immunostaining on OP (a) & MP (b) dorsal skin tissue samples at 400x magnification. Dermal dendritic cells were labelled with anti-CD11b antibody on OP (c) & MP samples (d) at 400x magnification. Image collected & cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/30842501), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Immunocytochemistry/ Immunofluorescence: CD11b Antibody - BSA Free [NB110-89474] - CD11b staining in IMhu. Cells were stained with antibodies against the CD11b surface antigen. (A) Panel A shows positive staining for CD11b & (B) panel B shows nuclear DAPI staining. Magnitude 40×. Image collected & cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/31096716), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Population of CD11b + myeloid progenitor cells differentiate into SMA + stromal cells within tumors and in vitro. (A) Representative image of red fluorescent protein (RFP) + stromal cells in tumor from CCR2-RFP heterozygous SCID mouse. (B) RFP + SMA + double positive cells within tumor stroma. (C) CD11b + SMA + double positive cells within tumor stroma. (D) CD45 + CD11b + CD34+ myeloid progenitor cells in the mammary gland at 1.5 (n = 5 empty vector (EV), 7 CCL2) and 2.5 weeks (n = 5 EV, 7 CCL2) post-transplantation were quantified by flow cytometry. (E) CD45 + CD11b + CD34 + myeloid progenitor cells in the bone marrow at 1.5 weeks (n = 6 EV, 7 CCL2) and 2.5 weeks (n = 3 mice/group) post-transplantation were quantified by flow cytometry. (F) Representative brightfield image of colony formed by CD45 + CD11b + CD34 + myeloid progenitor cells isolated using fluorescence-activated cell sorting (FACS). (G) Colonies in culture co-stained with SMA and collagen I. Statistical differences determined by Mann–Whitney U test. Magnification bars = 50 um. Image collected and cropped by CiteAb from the following open publication (//pubmed.ncbi.nlm.nih.gov/32731354), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Reactivity:

Hu, Mu, Rt, Bv, Ce, ChHa, Pm, RM

Species Glossary

Reactivity: Hu, Mu, Rt, Bv, Ce, ChHa, Pm, RM

Applications:

, , , , , , ,

Applications: , , , , , , ,

Host:

Rabbit Polyclonal

Host: Rabbit Polyclonal

Sizes:

Sample Size Available

Sizes: Sample Size Available

Conjugate:

Unconjugated

Available Conjugates:

Conjugate	Catalog #	Availability	Size	Price
Alexa Fluor 350	NB110-89474AF350
Alexa Fluor 405	NB110-89474AF405
Alexa Fluor 488	NB110-89474AF488
Alexa Fluor 532	NB110-89474AF532
Alexa Fluor 594	NB110-89474AF594
Alexa Fluor 647	NB110-89474AF647
Alexa Fluor 700	NB110-89474AF700
Alexa Fluor 750	NB110-89474AF750
Allophycocyanin	NB110-89474APC
Allophycocyanin/Cy7	NB110-89474APCCY7
Biotin	NB110-89474B
CoraFluor 1	NB110-89474CL1
DyLight 350	NB110-89474UV
DyLight 405	NB110-89474V
DyLight 488	NB110-89474G
DyLight 550	NB110-89474R
DyLight 594	NB110-89474DL594
DyLight 650	NB110-89474C
DyLight 680	NB110-89474FR
DyLight 755	NB110-89474IR
FITC	NB110-89474F
HRP	NB110-89474H
Janelia Fluor 525	NB110-89474JF525
Janelia Fluor 549	NB110-89474JF549
Janelia Fluor 646	NB110-89474JF646
Janelia Fluor 669	NB110-89474JF669
PE	NB110-89474PE
PE/Atto594	NB110-89474PEATT594
PE/Cy5.5	NB110-89474PECY55
PE/Cy7	NB110-89474PECY7
PerCP	NB110-89474PCP
mFluor Violet 450 SE	NB110-89474MFV450
mFluor Violet 500 SE	NB110-89474MFV500
mFluor Violet 610 SE	NB110-89474MFV610

Available Formulations

Formulation	Catalog #	Availability	Price
BSA Free	NB110-89474SS

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(select up to 3 products from this page to compare)

NB300-141

GFAP Antibody

(12 Reviews)

(117 Publications)

0.05 ml

NB300-141

Simple Western: GFAP Antibody [NB300-141] - Simple Western lane view shows a specific band for GFAP in 0.05 mg/mL of Human Brain lysate. This experiment was performed under reducing conditions using the 12-230 kDa separation system.

Immunocytochemistry/Immunofluorescence: GFAP Antibody [NB300-141] - The inhibition of Kv1.3 channels induces neuroprotection against the toxic effects of glioma. Immunofluorescence analyses of Kv1.3 expression (red) on GFAP-positive cells (green) in coronal brain slices of GL261-bearing mice in peritumoral region; in the magnification (right) arrows indicate co-expression of Kv1.3 and GFAP in the same cell. Image collected and cropped by CiteAb from the following publication (//www.nature.com/articles/s41598-018-25940-5) licensed under a CC-BY license.

Immunohistochemistry-Paraffin: GFAP Antibody [NB300-141] - Mouse brain section, 20x magnification. Antibody at 1:1000. Detection with Polymer-HRP. IHC image submitted by a verified customer review.

Western Blot: GFAP Antibody [NB300-141] - Analysis of Rat brain lysate. Antibody at 1:5000. Specific band running with an apparent SDS-PAGE molecular weight of ~50 kDa corresponds to rodent GFAP was observed.

Western Blot: GFAP Antibody [NB300-141] - Analysis of GFAP expression in whole rat cerebellum homogenate.

Western Blot: GFAP Antibody [NB300-141] - Analysis of different tissue lysates using rabbit polyclonal antibody to GFAP, NB300-141, dilution 1:5000 in green: [1] protein standard (red), [2] rat brain, [3] rat spinal cord, [4] mouse brain, [5] mouse spinal cord. Strong band at about 50 kDa corresponds to the major isotype of the GFAP protein. Smaller isotypes and proteolytic fragments of GFAP are also detected on the blot.

Immunocytochemistry/Immunofluorescence: GFAP Antibody [NB300-141] - Analysis of mixed neuron-glial cultures using GFAP antibody NB300-141 (red) and Vimentin antibody NB300-223 (green). The fibroblastic cells contain only Vimentin and so are green. The astrocytes contain either Vimentin and GFAP (appearing golden) or predominantly GFAP (appearing red). Blue is nuclear DNA stain.

Immunocytochemistry/Immunofluorescence: GFAP Antibody [NB300-141] - Cultured Rat hippocampal neurons. ICC/IF image submitted by a verified customer review.

Immunohistochemistry: GFAP Antibody [NB300-141] - Xenografted mouse brain section: astocyte and human nuclei. ICC/IF image submitted by a verified customer review.

Immunohistochemistry-Frozen: GFAP Antibody [NB300-141] - Imaging of mouse brain (cortex), 20x magnification. IHC image submitted by a verified customer review.

EGFP+ neurons are positive for RABV antigen.Brains were collected from Cre reporter mice fifteen days post-infection, cryosectioned, and EGFP+ regions compared to cell-specific labeling, A) NeuN (blue, neuronal nuclei antibody, 20× fluorescence imaging), B) GFAP (blue, astrocyte antibody, 40× confocal imaging), or C) RABV P antigen (purple) and DAPI nuclear stain (blue, 63× confocal imaging). White arrows in (C) indicate regions positive for RABV P.

Immunocytochemistry/ Immunofluorescence: GFAP Antibody [NB300-141] - EGFP+ neurons are positive for RABV antigen.Brains were collected from Cre reporter mice fifteen days post-infection, cryosectioned, & EGFP+ regions compared to cell-specific labeling, A) NeuN (blue, neuronal nuclei antibody, 20× fluorescence imaging), B) GFAP (blue, astrocyte antibody, 40× confocal imaging), or C) RABV P antigen (purple) & DAPI nuclear stain (blue, 63× confocal imaging). White arrows in (C) indicate regions positive for RABV P. Image collected & cropped by CiteAb from the following publication (//dx.plos.org/10.1371/journal.ppat.1002971), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Western Blot: GFAP Antibody [NB300-141] - Effects of the repeated administration of NVP CXCR2 20 (NVP; 10 μg/5 μl; i.t.; 16 h & 1 h before CCI & then once a day for 7 days) on the protein levels of CXCR2, IBA1, GFAP, CXCL1, CXCL2, & CXCL3 proteins (A–I) in the spinal cord (A–F) & DRG (G–I) on the 7th day after CCI in rats. The data are presented as the mean fold changes relative to the control ± SEM (5–6 samples per group). Intergroup differences were analyzed using ANOVA with Bonferroni's multiple comparisons test. *p < 0.05, **p < 0.01, ***p < 0.001 indicate differences vs. naive rats. #p < 0.05, indicate differences between V-treated & NVP-treated rats. CCI, chronic constriction injury; N, naive; V, vehicle; NVP, NVP CXCR2 20. Image collected & cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/31616413), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Immunocytochemistry/ Immunofluorescence: GFAP Antibody [NB300-141] - Increased astrocyte activation in IL-1 beta -stimulated two-week old offspring is reduced by maternal LB supplementation. Representative images of fluorescence microscopy of claudin-5+ (location of the brain capillaries, red), GFAP+ astrocyte (green), & DAPI (nuclei, blue). Three to five sections per mouse were examined & at least three mice were examined in each group. Stronger than control SPF GFAP staining was observed around the blood vessel (see arrow) after IL-1 beta insult. Maternal supplemented group (LB) with or without postnatal insult had GFAP levels similar to the control group indicating that LB supplementation prevented astrocyte activation around the BBB endothelium. Image collected & cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/32424168), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Immunocytochemistry/ Immunofluorescence: GFAP Antibody [NB300-141] - Glial cells density is differently modulated during AD progression.a Retinal slices were immunolabeled with anti-GFAP antibody (green) & Hoechst for nuclei visualization (blue) at different ages of 3xTg-AD & non-Tg mice & density of GFAP signal was quantified as shown in b (**p < 0.01 pre vs early; n = 16 fields/four slices for each condition; two-way ANOVA, Holm-Sidak; ##p < 0.01 for comparison with age-matched non-Tg mice, two-way ANOVA, Holm-Sidak). c Representative multiarea image of retinal slice immunolabeled with anti-Iba1 antibody (green) & Hoechst for nuclei visualization (blue); density of Iba1+ cells was quantified as shown in d (**p < 0.01 vs 3xTg-AD pre; ##p < 0.01 vs age-matched non-Tg mice, n = 16 fields/four slices for each condition, two-way ANOVA, Holm-Sidak method for multiple comparison) Image collected & cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/29880901), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Reactivity:

Hu, Mu, Rt, Po, Bv, Ch, Eq, Gp, Rb

Species Glossary

Reactivity: Hu, Mu, Rt, Po, Bv, Ch, Eq, Gp, Rb

Applications:

, , ,

Applications: , , ,

Host:

Rabbit Polyclonal

Host: Rabbit Polyclonal

Conjugate:

Unconjugated

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NB110-40763

TRPA1 Antibody - BSA Free

(2 Reviews)

(84 Publications)

0.1 ml

NB110-40763

Immunocytochemistry/Immunofluorescence: TRPA1 Antibody [NB110-40763] - Ai2 elicits TRPA1-dependent Ca2+ influx in astrocytes. Immunostaining of primary astrocytes from WT mice with anti-IgG and anti-TRPA1 antibody, then FITC-conjugated secondary antibody. Image collected and cropped by Citeab from the following publication (Role of transient receptor potential ankyrin 1 channels in Alzheimer's disease. J Neuroinflammation (2016)) licensed under a CC-BY license.

Flow Cytometry: TRPA1 Antibody [NB110-40763] - An intracellular stain was performed on A549 cells with NB110-40763C (blue) and a matched isotype control (orange). Cells were fixed with 4% PFA and then permeabilized with 0.1% saponin. Cells were incubated in an antibody dilution of 2.5 ug/mL for 30 minutes at room temperature. Both antibodies were conjugated to DyLight 650.

Flow Cytometry: TRPA1 Antibody [NB110-40763] - An intracellular stain was performed on A549 cells with NB110-40763G (blue) and a matched isotype control (orange). Cells were fixed with 4% PFA and then permeabilized with 0.1% saponin. Cells were incubated in an antibody dilution of 5 ug/mL for 30 minutes at room temperature. Both antibodies were conjugated to DyLight 488

Western Blot: TRPA1 Antibody [NB110-40763] - The essential role of TRPA1 in Ai2-induced calcium influx in HEK293 cells. (a) Western blot analysis of TRPA1 and I+--tubulin protein levels in non-treated, vector-or TRPA1-transfected HEK293 cells. Image collected and cropped by Citeab from the following publication (Role of transient receptor potential ankyrin 1 channels in Alzheimer's disease. J Neuroinflammation (2016)) licensed under a CC-BY license.

Immunocytochemistry/Immunofluorescence: TRPA1 Antibody [NB110-40763] - Analysis of TRPA1 in HEK 293 cells (Flp In Trex system) cells.

Western Blot: TRPA1 Antibody - BSA Free [NB110-40763] - Effects of Lycium barbarum polysaccharides (LBP) & capsaicin (CAP) on colonic (A) Cyclooxygenase-2 (COX-2), (B) Transient receptor potential cation channel V1 (TRPV1), & (C) Transient receptor potential ankyrin 1 (TRPA1) protein expression. (D) Representatives of Western blot for COX-2, TRPV1, TRPA1, & beta -actin. N: control group, U: ulcerative colitis induced group, L: LBP treated group, C: CAP treated group, M: mixed LBP & CAP treated group. Data are presented as mean ± SEM & analyzed by one-way ANOVA & Fisher’s least significant difference test (n = 8). # p < 0.05 compared to the N group. * p < 0.05 compared to the U group. Image collected & cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/35269566), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Immunocytochemistry/ Immunofluorescence: TRPA1 Antibody - BSA Free [NB110-40763] - Expression & localization of TRPA1 channels in wild-type (WT) & APP/PS1 Tg mice. (a) Brains were harvested from WT & APP/PS1 Tg mice at 8 months old. Western blot analysis of protein levels of TRPA1 & alpha -tubulin. Data are mean ± SEM from 6 mice in each group. *, P < 0.05 vs. WT mice. (b, c) Immunohistochemistry of specimens of cortex & hippocampus from 8-month-old WT & APP/PS1 Tg mice with the antibodies anti-TRPA1, anti-vWF (endothelial cell marker), anti-NeuN (neuron marker), anti-GFAP (astrocyte marker) & anti-IBA-1 (microglia marker), then FITC- or Texas red-conjugated secondary antibody. Bar = 50 μm. vWF-positive cells denoted endothelial cells, NeuN-positive cells denoted neurons, & GFAP-positive cells denoted astrocytes, as indicated by arrowheads, stars or arrows, respectively Image collected & cropped by CiteAb from the following publication (//jneuroinflammation.biomedcentral.com/articles/10.1186/s12974-016-0557-z), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

$Immunocytochemistry/ Immunofluorescence: TRPA1 Antibody - BSA Free [NB110-40763] - Evaluation of anti-TRPA1 antibody specificity by western blotting & immunofluorescence. (a) Lysates derived from HEK293T cells transiently transfected with the TRPA1 & GFP expression construct (TRPA1 OE) or TRPM2 & GFP negative control (TRPM2 OE) were probed with the antibodies indicated. Additional untransfected & GFP only controls are presented in the first blot (6G8). Uncropped full length blots are displayed, gaps between the blots are present to indicate the use of a different antibody. Mouse mAbs C-5 & 6G8, & NB110-40763 can detect TRPA1 only in the membrane fraction of lysates at the expected molecular weight (127.5 kDa). Several TRPA1-specific bands are observed above this weight. NB110-40763 also detects several other antigens. Ab58844 & ACC- 037 only appear to detect antigens other than TRPA1 in the conditions used. (b) The performance of the same antibodies was evaluated by immunofluorescence (red) in comparison to the expression of the GFP reporter (green), or control TRPM2 & GFP overexpressing cells as for western blotting. Mouse mAb C-5 again shows high specificity with a strong correlation between the expression of the GFP reporter & antibody staining, & no staining in TRPM2 & GFP overexpressing controls. NB110-40763 also demonstrates some sensitivity but has high background that likely does not correspond to Fc binding of the antibody, as the other two rabbit polyclonal antibodies or isotype control did show different staining patterns. Ab58844 & ACC- 037 only appear to detect antigens other than TRPA1 in the conditions used. Image collected & cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/31811235), licensed under a CC-BY license. Not internally tested by Novus Biologicals.$

Western Blot: TRPA1 Antibody - BSA Free [NB110-40763] - Expression & localization of TRPA1 channels in wild-type (WT) & APP/PS1 Tg mice. (a) Brains were harvested from WT & APP/PS1 Tg mice at 8 months old. Western blot analysis of protein levels of TRPA1 & alpha -tubulin. Data are mean ± SEM from 6 mice in each group. *, P < 0.05 vs. WT mice. (b, c) Immunohistochemistry of specimens of cortex & hippocampus from 8-month-old WT & APP/PS1 Tg mice with the antibodies anti-TRPA1, anti-vWF (endothelial cell marker), anti-NeuN (neuron marker), anti-GFAP (astrocyte marker) & anti-IBA-1 (microglia marker), then FITC- or Texas red-conjugated secondary antibody. Bar = 50 μm. vWF-positive cells denoted endothelial cells, NeuN-positive cells denoted neurons, & GFAP-positive cells denoted astrocytes, as indicated by arrowheads, stars or arrows, respectively Image collected & cropped by CiteAb from the following publication (//jneuroinflammation.biomedcentral.com/articles/10.1186/s12974-016-0557-z), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Reactivity:

Hu, Mu, Rt, Gp, Ze

Species Glossary

Reactivity: Hu, Mu, Rt, Gp, Ze

Applications:

, , , ,

Applications: , , , ,

Host:

Rabbit Polyclonal

Host: Rabbit Polyclonal

Sizes:

Sample Size Available

Sizes: Sample Size Available

Conjugate:

Unconjugated

Available Conjugates:

Conjugate	Catalog #	Availability	Size	Price
Alexa Fluor 350	NB110-40763AF350
Alexa Fluor 405	NB110-40763AF405
Alexa Fluor 488	NB110-40763AF488
Alexa Fluor 532	NB110-40763AF532
Alexa Fluor 594	NB110-40763AF594
Alexa Fluor 647	NB110-40763AF647
Alexa Fluor 700	NB110-40763AF700
Alexa Fluor 750	NB110-40763AF750
Allophycocyanin	NB110-40763APC
Allophycocyanin/Cy7	NB110-40763APCCY7
Biotin	NB110-40763B
CoraFluor 1	NB110-40763CL1
DyLight 350	NB110-40763UV
DyLight 405	NB110-40763V
DyLight 488	NB110-40763G
DyLight 550	NB110-40763R
DyLight 594	NB110-40763DL594
DyLight 650	NB110-40763C
DyLight 680	NB110-40763FR
DyLight 755	NB110-40763IR
FITC	NB110-40763F
HRP	NB110-40763H
Janelia Fluor 525	NB110-40763JF525
Janelia Fluor 549	NB110-40763JF549
Janelia Fluor 646	NB110-40763JF646
Janelia Fluor 669	NB110-40763JF669
PE	NB110-40763PE
PE/Atto594	NB110-40763PEATT594
PE/Cy5.5	NB110-40763PECY55
PE/Cy7	NB110-40763PECY7
PerCP	NB110-40763PCP
mFluor Violet 450 SE	NB110-40763MFV450
mFluor Violet 500 SE	NB110-40763MFV500
mFluor Violet 610 SE	NB110-40763MFV610

Available Formulations

Formulation	Catalog #	Availability	Price
BSA Free	NB110-40763SS

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NBP2-13075

beta Amyloid Antibody (MOAB-2) - BSA Free

(2 Reviews)

(75 Publications)

0.1 ml

NBP2-13075

IHC analysis of beta Amyloid on normal mouse brain (left) and 5xFAD mouse brain (right) using DAB with hematoxylin counterstain. The MOAB-2 antibody was used at 1:20 on normal mouse brain and at 1:400 on 5xFAD mouse brain.

Analysis of beta Amyloid (MOAB-2) antibody in (1) 100 pmole beta Amyloid 42, (2) 5xFAD mouse brain homogenate Repetition 1 and (3) 5xFAD mouse brain homogenate Repetition 2.

Western blot analysis in cell lysates from HEK-APP SWE/BACE1 cells probed with an antibody against the C-terminus of APP (Lanes 1 and 2) and beta Amyloid (MOAB-2, Lanes 3 and 4). Beta Amyloid (MOAB-2) does not detect APP (from PMID: 22423893).

IHC analysis of a formalin fixed paraffin embedded tissue section of human brain (Alzheimers disease, hippocampus) using 1:200 dilution of anti-beta Amyloid antibody (clone MOAB-2). The staining was developed with HRP labeled anti-mouse secondary antibody and DAB reagent, and nuclei of cells were counter-stained with hematoxylin. This beta Amyloid antibody specifically stained the cells with Abeta 42/ Abeta aggregates while the normal cells were negative for abeta peptide.

Immunofluorescent detection of beta Amyloid with MOAB-2 in the subiculim of 1-, 2- and 4- month old 5xFAD mice. Scale bar 20 um (from PMID: 22423893).

A plaque load in neocortex and hippocampus in APP/PS1 mice exposed to differential housing. Representative 10x MOAB-2 staining in hippocampus of APP/PS1 mice for each housing group. Image collected and cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/28584278/) licensed under a CC-BY license.

IHC analysis of a formalin fixed paraffin embedded tissue section of human brain (Alzheimers disease, hippocampus) using 1:40 dilution of anti-beta Amyloid antibody (clone MOAB-2). The staining was developed with HRP labeled anti-mouse secondary antibody and DAB reagent, and nuclei of cells were counter-stained with hematoxylin. This beta Amyloid antibody specifically stained the cells with Abeta 42/ Abeta aggregates while the normal cells were negative for abeta peptide.

Mouse brain (cerebral cortex). Red: MOAB-2 antibody staining, Blue: DAPI. Zeiss LSM800, 40x. Image from verified customer review.

Immunocytochemistry/ Immunofluorescence: beta Amyloid Antibody (MOAB-2) - BSA Free [NBP2-13075] - No difference in A beta plaque load between propofol (n = 8) & vehicle (n = 6) treated APP/PS1 mice. a An example image of A beta plaque immunoreactivity in the cortex of an APP/PS1 mouse following repeated propofol exposure. b A representative image of A beta plaque immunolabeling the cortex of an APP/PS1 mouse following treatment with vehicle. c Bar graph showing the percentage of the cortex occupied by A beta plaques in propofol & vehicle treated APP/PS1 mice. d Bar graph showing the average size (μm2) of A beta plaques in the cortex of APP/PS1 in the propofol & vehicle treatment groups. e Bar graph showing the average density of A beta plaques (/μm2) in the cortex of propofol & vehicle exposed APP/PS1 mice. All data is shown as mean ± SEM. Scale bar = 500 μm Image collected & cropped by CiteAb from the following publication (//bmcanesthesiol.biomedcentral.com/articles/10.1186/s12871-018-0509-5), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Murine brain cryosections stained with primary MOAB-2 antibody followed by a secondary donkey anti-mouse antibody. Image from a verified customer review.

Reactivity:

Hu, Mu, Rt, Ba, Pm

Species Glossary

Reactivity: Hu, Mu, Rt, Ba, Pm

Applications:

, , , , , , ,

Applications: , , , , , , ,

Host:

Mouse Monoclonal

Host: Mouse Monoclonal

Sizes:

Sample Size Available

Sizes: Sample Size Available

Conjugate:

Unconjugated

Available Conjugates:

Conjugate	Catalog #	Availability	Size	Price
Alexa Fluor 350	NBP2-13075AF350
Alexa Fluor 405	NBP2-13075AF405
Alexa Fluor 488	NBP2-13075AF488
Alexa Fluor 532	NBP2-13075AF532
Alexa Fluor 647	NBP2-13075AF647
Alexa Fluor 700	NBP2-13075AF700
Alexa Fluor 750	NBP2-13075AF750
Allophycocyanin	NBP2-13075APC
Biotin	NBP2-13075B
CoraFluor 1	NBP2-13075CL1
DyLight 350	NBP2-13075UV
DyLight 405	NBP2-13075V
DyLight 488	NBP2-13075G
DyLight 550	NBP2-13075R
DyLight 594	NBP2-13075DL594
DyLight 650	NBP2-13075C
DyLight 680	NBP2-13075FR
DyLight 755	NBP2-13075IR
FITC	NBP2-13075F
HRP	NBP2-13075H
Janelia Fluor 525	NBP2-13075JF525
Janelia Fluor 549	NBP2-13075JF549
Janelia Fluor 646	NBP2-13075JF646
Janelia Fluor 669	NBP2-13075JF669
PE	NBP2-13075PE
PerCP	NBP2-13075PCP
mFluor Violet 450 SE	NBP2-13075MFV450
mFluor Violet 500 SE	NBP2-13075MFV500
mFluor Violet 610 SE	NBP2-13075MFV610

Available Formulations

Formulation	Catalog #	Availability	Price
BSA Free	NBP2-13075SS
Azide and BSA Free	NBP2-80594

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NB100-2324

IRE1 alpha Antibody - BSA Free

(2 Reviews)

(64 Publications)

0.1 ml

NB100-2324

Western Blot: IRE1 alpha Antibody [NB100-2324] - ALOX15 knockout blocks alcohol-induced up-regulation of IRE1a in mouse liver. Image from verified customer review.

Immunocytochemistry/Immunofluorescence: IRE1 alpha Antibody [NB100-2324] - IRE-1 alpha antibody was tested in HeLa cells at 1:200 against Dylight 488 (Green). Alpha tubulin and nuclei were counterstained against Dylight 568 (Red) and DAPI (Blue).

Immunohistochemistry-Paraffin: IRE1 alpha Antibody [NB100-2324] - Analysis of a formalin fixed mouse colon tissue section using total IRE1 alpha antibody (NB100-2324) at 1:300. Note a strong cytoplasmic signal in various cells of colonic villi (columnar epithelial and goblet cells) and the muscular layer. A few cells, potentially with active UPR, showed nuclear positivity also while the signal was negligible in cells at base of crypts and lamina propria.

The inositol-requiring enzyme 1 alpha (IRE1 alpha )/ X-box-binding-protein 1 spliced isoform (XBP1s) arm of unfolded protein response (UPR) is induced by angiotensin II in VSMCs. (A–C) The rat aortic VSMCs infected with adenovirus encoding GRP78 or control GFP (100 moi) for 48 h were stimulated with 100 nM AngII (AII) for 1–6 h & immunoblotting was performed as indicated. (A) Representative blots from 4 independent experiments. (B) Signal intensity was used to calculate the expression ratio of XBP1s to GAPDH. (C) Signal intensity was used to calculate the IRE1 alpha Ser724 phosphorylation ratio to the total IRE1 alpha . The bars in the graphs show the mean ± SD from 4 independent experiments. * indicates p < 0.05. Image collected & cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/32679678), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Abnormal Paneth cells show ER stress.(A, B) Representative transmission electron microscopy images of Paneth cells at the base of ileal crypts in (A) ICR & (B) SAMP1/YitFc mice. Scale bars indicate 2 μm. (C, D) Quantitative analysis of (C) granule number & (D) ER lumen diameter in Paneth cells (n = 3/each week for SAMP1/YitFc mice). For the measurements, three Paneth cells were randomly selected from each mouse. (E) SDS–PAGE Western blot analysis of ER stress markers, pIRE1 alpha , ATF4, cleaved-ATF6, & GRP78 in ileal crypts (n = 4/each group). Total-IRE1 alpha & HPRT1 was used as loading control. (F) Relative expression level of ER stress markers calculated from the band intensity. Error bars represent mean ± SEM. (C, D, F) Statistical significance was evaluated by t test in (C, D), & one-way ANOVA followed by Tukey’s post hoc test in (F). P < 0.05 was considered statistically significant. *P < 0.05, †P < 0.01, §P < 0.001. E, ER; G, granules; N, nucleus; n.s., not significant. Image collected & cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/32345659), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Western Blot: IRE1 alpha Antibody [NB100-2324] - Zn (II)-curc induces endoplasmic reticulum (ER) stress in mutant p53H273-carrying cells. (a) Representative photomicrographs of ER-Red Fluorescence staining in U373 cells untreated (Mock) or treated with Zn (II)-curc (100 µg/mL) for 16 h (Original magnification: 40×). (b) Quantization of ER content in U373 cells from ER-Red Fluorescence-stained cells. Mean fluorescence intensity (MFI) of each individual cell was normalized to cell size & expressed as fold-change compared with untreated cells at the same time point. Histograms represent the mean ± SD of three independent experiments. * p ≤ 0.05. (c) Western blot analysis of p53, BiP, total (tot) IRE1 alpha , phosphorylated (p) IRE1 alpha , & XBP1 spliced (s) protein levels evaluated in U373 & HT29 cells untreated or treated with Zn (II)-curc (100 µg/mL) for 24 h. (d) Densitometric analysis was performed using Image J software to calculate the ratio of the protein levels, as detected in (c), vs. beta -actin. Histograms represent the mean ± SD of three independent experiments. * p ≤ 0.05. (e) Total mRNA was extracted from U373 & HT29 cells untreated or treated with Zn (II)-curc (100 µg/mL) for 24 h. Spliced (s) Xbp1 gene expression was assayed by the polymerase chain reaction (PCR) of reverse-transcribed cDNA. Densitometric analysis was performed using Image J software to calculate the Xbp1s/28S ratio. Histograms represent the mean ± SD of three independent experiments. * p ≤ 0.05. (f) p53 gene expression was assayed by PCR as in (e). The p53/28S ratio is indicated. Image collected & cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/32138264), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Reactivity:

Hu, Mu, Rt

Species Glossary

Reactivity: Hu, Mu, Rt

Applications:

, , , ,

Applications: , , , ,

Host:

Rabbit Polyclonal

Host: Rabbit Polyclonal

Sizes:

Sample Size Available

Sizes: Sample Size Available

Conjugate:

Unconjugated

Available Conjugates:

Validated by:

Validated by:

Conjugate	Catalog #	Availability	Size	Price
Alexa Fluor 350	NB100-2324AF350
Alexa Fluor 405	NB100-2324AF405
Alexa Fluor 488	NB100-2324AF488
Alexa Fluor 532	NB100-2324AF532
Alexa Fluor 594	NB100-2324AF594
Alexa Fluor 647	NB100-2324AF647
Alexa Fluor 700	NB100-2324AF700
Alexa Fluor 750	NB100-2324AF750
Allophycocyanin	NB100-2324APC
Biotin	NB100-2324B
CoraFluor 1	NB100-2324CL1
DyLight 350	NB100-2324UV
DyLight 405	NB100-2324V
DyLight 488	NB100-2324G
DyLight 550	NB100-2324R
DyLight 594	NB100-2324DL594
DyLight 650	NB100-2324C
DyLight 680	NB100-2324FR
DyLight 755	NB100-2324IR
FITC	NB100-2324F
HRP	NB100-2324H
Janelia Fluor 525	NB100-2324JF525
Janelia Fluor 549	NB100-2324JF549
Janelia Fluor 646	NB100-2324JF646
Janelia Fluor 669	NB100-2324JF669
PE	NB100-2324PE
PerCP	NB100-2324PCP
mFluor Violet 450 SE	NB100-2324MFV450
mFluor Violet 500 SE	NB100-2324MFV500
mFluor Violet 610 SE	NB100-2324MFV610

Available Formulations

Formulation	Catalog #	Availability	Price
BSA Free	NB100-2324SS

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NB100-77417

CD45 Antibody (30-F11) - BSA Free

(5 Reviews)

(48 Publications)

0.5 mg

NB100-77417

Immunohistochemistry-Paraffin: CD45 Antibody (30-F11) [NB100-77417] - Mouse glomeruli stained with CD45 antibody. 4% formaldehyde fixed paraffin sections. EDTA was used for antigen retrieval. IHC-P image submitted by a verified customer review.

Immunohistochemistry: CD45 Antibody (30-F11) [NB100-77417] - Analysis of a FFPE embedded tissue section of mouse liver using 1:100 dilution of CD45 antibody (30-F11) [NB100-77417]. The signal was developed using AEC reagent based method with hematoxylin counterstaining.

Immunohistochemistry-Frozen: CD45 Antibody (30-F11) [NB100-77417] - Analysis of a mouse spleen cryosection using CD45 antibody (30-F11) [NB100-77417] at 1:50 dilution. The signal was detected using goat anti-rat Alexa fluor 488 secondary with DAPI counterstaining. IHC-P image submitted by a verified customer review.

Immunohistochemistry-Paraffin: CD45 Antibody (30-F11) [NB100-77417] - Staining of a FFPE mouse liver tissue section using 1:100 dilution of CD45 antibody (30-F11) [NB100-77417]. Signal was detected using AF488 conjugated donkey anti-rat secondary antibody at 1:500 dilution. IHC-P image submitted by a verified customer review.

Immunohistochemistry: CD45 Antibody (30-F11) [NB100-77417] - Severe apoptosis and pathology in the orally infected heart. Experimental design is as outlined in Fig. 1B. Heart sections from moribund mice were examined with H&E, and immunohistochemistry staining for pan-leukocyte infiltration using an anti-CD45 antibody. Image collected and cropped by CiteAb from the following publication (//www.nature.com/articles/s41598-019-47455-3), licensed under a CC-BY license.

Immunohistochemistry: CD45 Antibody (30-F11) [NB100-77417] - VP1-positive infiltrating M2 macrophage and VP1-positive pneumocytes were detectable in the orally infected lung. Adjacent lung sections were examined with H&E and IHC staining for a pan-leukocyte marker CD45. Image collected and cropped by CiteAb from the following publication (//www.nature.com/articles/s41598-019-47455-3), licensed under a CC-BY license.

Reactivity:

Hu, Mu, Rt

Species Glossary

Reactivity: Hu, Mu, Rt

Applications:

, , , , , ,

Applications: , , , , , ,

Host:

Rat Monoclonal

Host: Rat Monoclonal

Sizes:

Sample Size Available

Sizes: Sample Size Available

Conjugate:

Unconjugated

Available Conjugates:

Conjugate	Catalog #	Availability	Size	Price
Alexa Fluor 350	NB100-77417AF350
Alexa Fluor 405	NB100-77417AF405
Alexa Fluor 488	NB100-77417AF488
Alexa Fluor 532	NB100-77417AF532
Alexa Fluor 594	NB100-77417AF594
Alexa Fluor 647	NB100-77417AF647
Alexa Fluor 700	NB100-77417AF700
Alexa Fluor 750	NB100-77417AF750
Allophycocyanin	NB100-77417APC
Biotin	NB100-77417B
CoraFluor 1	NB100-77417CL1
DyLight 350	NB100-77417UV
DyLight 405	NB100-77417V
DyLight 488	NB100-77417G
DyLight 550	NB100-77417R
DyLight 594	NB100-77417DL594
DyLight 650	NB100-77417C
DyLight 680	NB100-77417FR
DyLight 755	NB100-77417IR
FITC	NB100-77417F
HRP	NB100-77417H
Janelia Fluor 525	NB100-77417JF525
Janelia Fluor 549	NB100-77417JF549
Janelia Fluor 646	NB100-77417JF646
Janelia Fluor 669	NB100-77417JF669
PE	NB100-77417PE
PerCP	NB100-77417PCP
mFluor Violet 450 SE	NB100-77417MFV450
mFluor Violet 500 SE	NB100-77417MFV500
mFluor Violet 610 SE	NB100-77417MFV610

Available Formulations

Formulation	Catalog #	Availability	Price
Azide and BSA Free	NBP2-80652-0.1mg
BSA Free	NB100-77417SS
Azide and BSA Free	NBP2-80652

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NBP1-05198

GFAP Antibody - BSA Free

(1 Review)

(52 Publications)

0.1 ml

NBP1-05198

Reactivity:

Hu, Mu, Rt, Po, Bv, Eq

Species Glossary

Reactivity: Hu, Mu, Rt, Po, Bv, Eq

Applications:

, , ,

Applications: , , ,

Host:

Chicken Polyclonal

Host: Chicken Polyclonal

Sizes:

Sample Size Available

Sizes: Sample Size Available

Conjugate:

Unconjugated

Available Formulations

Formulation	Catalog #	Availability	Price
BSA Free	NBP1-05198-0.025ml

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At	=	A. thaliana	SyHa	=	Golden Syrian Hamster
All	=	All Species	Ha	=	Hamster
An	=	Animal	Hu	=	Human
ArHa	=	Armenian Hamster	I	=	Insect
Av	=	Avian	Ll	=	Llama
Bb	=	Baboon	Ma	=	Mammal
Ba	=	Bacteria	Mk	=	Monkey
Bv	=	Bovine	Mu	=	Mouse
Ca	=	Canine	Multi	=	Multi-species
Ce	=	C. Elegans	NA	=	Non-species specific
Ch	=	Chicken	Or	=	Orangutan
ChHa	=	Chinese Hamster	Pl	=	Plant
Cm	=	Cynomolgus Monkey	Pm	=	Primate
Do	=	Donkey	Po	=	Porcine
Dr	=	Drosophilia	Rb	=	Rabbit
Ec	=	E. Coli	Rt	=	Rat
Eq	=	Equine	RM	=	Rhesus Macaque
Fe	=	Feline	Sh	=	Sheep
Ft	=	Ferret	Vb	=	Vertebrate
Fi	=	Fish	Vi	=	Virus
Fu	=	Fungi	Xp	=	Xenopus
Ge	=	Gerbil	Ye	=	Yeast
GP	=	Guinea Pig	Ze	=	Zebrafish
Gt	=	Goat

Category

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Reactivity

Citation

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Available Conjugates

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Clonality

Clone

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Species Glossary

AIF-1/Iba1 Antibody

ABCA1 Antibody - BSA Free

IRE1 alpha [p Ser724] Antibody - BSA Free

ABCG1 Antibody - BSA Free

iNOS Antibody - BSA Free

CD11b Antibody - BSA Free

GFAP Antibody

TRPA1 Antibody - BSA Free

beta Amyloid Antibody (MOAB-2) - BSA Free

IRE1 alpha Antibody - BSA Free

CD45 Antibody (30-F11) - BSA Free

GFAP Antibody - BSA Free