Transgelin/TAGLN/SM22 alpha Antibody - BSA Free

Immunocytochemistry/Immunofluorescence: Transgelin/TAGLN/SM22 alpha Antibody [NBP1-33003] - HeLa cells were fixed in 4% paraformaldehyde at RT for 15 min. Green: Transgelin protein stained by Transgelin antibody diluted at 1:500. Red: alpha Tubulin, a cytoskeleton marker, stained by alpha Tubulin antibody [GT114] diluted at 1:1000. Blue: Hoechst 33342 staining.

Immunohistochemistry-Paraffin: Transgelin/TAGLN/SM22 alpha Antibody [NBP1-33003] - Mouse smooth muscle. Transgelin stained by Transgelin antibody diluted at 1:500.Antigen Retrieval: Citrate buffer, pH 6.0, 15 min.

Western Blot: Transgelin/TAGLN/SM22 alpha Antibody [NBP1-33003] - 30 ug C8D30 whole cell lysate/extract 12% SDS-PAGE gel, antibody dilution 1:1000.

Western Blot: Transgelin/TAGLN/SM22 alpha Antibody [NBP1-33003] - A. 30 ug Rat-2 whole cell lysate/extract 12 % SDS-PAGE Transgelin antibody dilution: 1:5000

Western Blot: Transgelin/TAGLN/SM22 alpha Antibody [NBP1-33003] - Non-transfected (-) and transfected (+) HeLa whole cell extracts (15 ug) were separated by 12% SDS-PAGE, and the membrane was blotted with Transgelin antibody.

Immunohistochemistry-Paraffin: Transgelin/TAGLN/SM22 alpha Antibody [NBP1-33003] - Rat stomach. Transgelin antibody diluted at 1:500. Antigen Retrieval: Citrate buffer, pH 6.0, 15 min

Western Blot: Transgelin/TAGLN/SM22 alpha Antibody [NBP1-33003] -Various whole cell extracts (30 ug) were separated by 12% SDS-PAGE, and the membrane was blotted with Transgelin antibody diluted at 1:1000. The HRP-conjugated anti-rabbit IgG antibody (NBP2-19301 was used to detect the primary antibody.

Various whole cell extracts (30 ug) were separated by 12% SDS-PAGE, and the membrane was blotted with Transgelin antibody (NBP1-33003) diluted at 1:1000. The HRP-conjugated anti-rabbit IgG antibody was used to detect the primary antibody.

MAP4K4 deficiency induces TGF beta /smad signaling and EndMT via activation of integrin beta 1. (a) HMVECs were transfected with MAP4K4 siRNA (100 nM) for 48 h. Next, the cells were treated with or without AcSDKP for 2 h. The p-smad3/smad3 pathway was analyzed by western blot. Densitometric analysis of the p-smad3/smad3 levels was performed, with n=3 for each group. (b) HMVECs were treated with MAP4K4 siRNA for 48 h with or without AcSDKP treatment. The VE-cadherin, CD31, FSP1, SM22 alpha and vimentin protein levels were analyzed by western blot. (c) HMVECs were transfected with MAP4K4 siRNA for 48 h in the presence or absence of TGF beta 2 with or without AcSDKP. The integrin beta 1 level was analyzed by western blot Image collected and cropped by CiteAb from the following open publication (//pubmed.ncbi.nlm.nih.gov/28771231), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

AcSDKP suppresses TGF beta /smad signaling and EndMT through the FGFR1/FRS2 pathway. (a) HMVECs were treated with N-FGFR1 for 48 h, and the FGFR1, TGF beta R1 and TGF beta R2 protein levels were analyzed by western blot. (b) HMVECs were treated with TGF beta 2 in the presence or absence of N-FGFR1 for 15 min with or without AcSDKP preincubation. The p-smad3 and TGF beta R1 protein levels were analyzed by western blot. Densitometric analysis of the p-smad3/smad3 and TGF beta R1/ beta -actin levels (n=3) in each group was performed. (c) HMVECs were incubated with either N-FGFR1 in the presence or absence of TGF beta 2 for 48 h with or without preincubation with AcSDKP for 2 h or with N-FGFR1 in the presence or absence of TGF beta 2 for 48 h with or without 24 h of incubation with FGF2 (50 ng/ml). The CD31, SM22 alpha , FSP1 and alpha -SMA protein levels were analyzed by western blot. (d) HMVECs were transfected with FRS2 siRNA (100 nM) for 48 h with or without AcSDKP preincubation. The VE-cadherin, FSP1, vimentin, SM22 alpha and p-smad3 levels were analyzed by western blot. (e) HMVECs were treated with N-FGFR1 for 48 h or 15 min in the presence or absence of N-TGF beta (1, 2, 3) (1.0 μg/ml). The CD31, VE-cadherin, SM22 alpha , FSP1, TGF beta R1, TGF beta R2 and p-smad3 levels were analyzed by western blot Image collected and cropped by CiteAb from the following open publication (//pubmed.ncbi.nlm.nih.gov/28771231), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

AcSDKP suppresses TGF beta /smad signaling and EndMT through the FGFR1/FRS2 pathway. (a) HMVECs were treated with N-FGFR1 for 48 h, and the FGFR1, TGF beta R1 and TGF beta R2 protein levels were analyzed by western blot. (b) HMVECs were treated with TGF beta 2 in the presence or absence of N-FGFR1 for 15 min with or without AcSDKP preincubation. The p-smad3 and TGF beta R1 protein levels were analyzed by western blot. Densitometric analysis of the p-smad3/smad3 and TGF beta R1/ beta -actin levels (n=3) in each group was performed. (c) HMVECs were incubated with either N-FGFR1 in the presence or absence of TGF beta 2 for 48 h with or without preincubation with AcSDKP for 2 h or with N-FGFR1 in the presence or absence of TGF beta 2 for 48 h with or without 24 h of incubation with FGF2 (50 ng/ml). The CD31, SM22 alpha , FSP1 and alpha -SMA protein levels were analyzed by western blot. (d) HMVECs were transfected with FRS2 siRNA (100 nM) for 48 h with or without AcSDKP preincubation. The VE-cadherin, FSP1, vimentin, SM22 alpha and p-smad3 levels were analyzed by western blot. (e) HMVECs were treated with N-FGFR1 for 48 h or 15 min in the presence or absence of N-TGF beta (1, 2, 3) (1.0 μg/ml). The CD31, VE-cadherin, SM22 alpha , FSP1, TGF beta R1, TGF beta R2 and p-smad3 levels were analyzed by western blot Image collected and cropped by CiteAb from the following open publication (//pubmed.ncbi.nlm.nih.gov/28771231), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

AcSDKP suppresses TGF beta /smad signaling and EndMT through the FGFR1/FRS2 pathway. (a) HMVECs were treated with N-FGFR1 for 48 h, and the FGFR1, TGF beta R1 and TGF beta R2 protein levels were analyzed by western blot. (b) HMVECs were treated with TGF beta 2 in the presence or absence of N-FGFR1 for 15 min with or without AcSDKP preincubation. The p-smad3 and TGF beta R1 protein levels were analyzed by western blot. Densitometric analysis of the p-smad3/smad3 and TGF beta R1/ beta -actin levels (n=3) in each group was performed. (c) HMVECs were incubated with either N-FGFR1 in the presence or absence of TGF beta 2 for 48 h with or without preincubation with AcSDKP for 2 h or with N-FGFR1 in the presence or absence of TGF beta 2 for 48 h with or without 24 h of incubation with FGF2 (50 ng/ml). The CD31, SM22 alpha , FSP1 and alpha -SMA protein levels were analyzed by western blot. (d) HMVECs were transfected with FRS2 siRNA (100 nM) for 48 h with or without AcSDKP preincubation. The VE-cadherin, FSP1, vimentin, SM22 alpha and p-smad3 levels were analyzed by western blot. (e) HMVECs were treated with N-FGFR1 for 48 h or 15 min in the presence or absence of N-TGF beta (1, 2, 3) (1.0 μg/ml). The CD31, VE-cadherin, SM22 alpha , FSP1, TGF beta R1, TGF beta R2 and p-smad3 levels were analyzed by western blot Image collected and cropped by CiteAb from the following open publication (//pubmed.ncbi.nlm.nih.gov/28771231), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

KLB deficiency led to EndMT in HMVECs. (A) Subconfluent HMVECs were transfected with KLB siRNA or control siRNA. Six hours later, the medium was replaced with an experimental medium, followed by N‐FGFR1 (1.5 mg·mL−1) treatment. At 48 h, the cells were harvested for western blot analysis. The results are from three repeated experiments. (B) The same treated HMVECs (as in A) cultured on 8‐well culture slides were subjected to immunofluorescence staining with an anti‐ alpha ‐SMA antibody and DAPI (scale bar, 100 μm). Six different fields were observed for each slide. (C) HMVECs with or without preincubation with AcSDKP (100 nm) for 2 h were transfected with KLB siRNA or control siRNA for 48 h. The expression of EndMT markers, including VE‐cadherin, alpha ‐SMA, vimentin, and SM22 alpha , was assessed by western blotting and quantified (D) by imagej software (GE Healthcare Life Sciences, Uppsala, Sweden). The data represent mean +/- SD and are representative of three independent experiments. One‐way ANOVA with Tukey's multiple comparisons test was used for statistical analysis. Image collected and cropped by CiteAb from the following open publication (//pubmed.ncbi.nlm.nih.gov/30972974), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

• Reactivity: Hu, Mu, Rt, Po, Bv
• Applications: WB, ICC/IF, IHC, IP
• Clonality: Polyclonal
• Host: Rabbit
• Conjugate: Unconjugated
• Format: BSA Free

Transgelin/TAGLN/SM22 alpha Antibody - BSA Free Summary

• Immunogen: Recombinant protein encompassing a sequence within the center region of human Transgelin/TAGLN/SM22 alpha. The exact sequence is proprietary.
• Localization: Cytoplasm
• Predicted Species: Porcine (98%), Bovine (97%). Backed by our 100% Guarantee.
• Isotype: IgG
• Clonality: Polyclonal
• Host: Rabbit
• Gene: TAGLN
• Purity: Antigen Affinity-purified

Applications/Dilutions

• Dilutions:
  • Immunocytochemistry/ Immunofluorescence 1:100-1:1000
  • Immunohistochemistry 1:100-1:1000
  • Immunohistochemistry-Paraffin 1:100-1:1000
  • Immunoprecipitation 1:100-1:500
  • Western Blot 1:500-1:10000
• Theoretical MW: 23 kDa.
  Disclaimer note: The observed molecular weight of the protein may vary from the listed predicted molecular weight due to post translational modifications, post translation cleavages, relative charges, and other experimental factors.

Reactivity Notes

Immunogen displays the following percentage of sequence identity for non-tested species: Chicken (85%).

Packaging, Storage & Formulations

• Storage: Aliquot and store at -20C or -80C. Avoid freeze-thaw cycles.
• Buffer: PBS, 1% BSA, 20% Glycerol
• Preservative: 0.025% Proclin 300
• Purity: Antigen Affinity-purified

Alternate Names for Transgelin/TAGLN/SM22 alpha Antibody - BSA Free

• DKFZp686P11128
• Protein WS3-10
• SM22 alpha
• SM2222 kDa actin-binding protein
• SMCCDKFZp686B01212
• Smooth muscle protein 22-alpha
• TAGLN
• TAGLN1
• transgelin variant 2
• Transgelin
• WS3-10
• WS3-10SM22-alpha

Background

The protein encoded by this gene is a transformation and shape-change sensitive actin cross-linking/gelling protein found in fibroblasts and smooth muscle. Its expression is down-regulated in many cell lines, and this down-regulation may be an early and sensitive marker for the onset of transformation. A functional role of this protein is unclear. Two transcript variants encoding the same protein have been found for this gene. [provided by RefSeq]

Limitations

This product is for research use only and is not approved for use in humans or in clinical diagnosis. Primary Antibodies are guaranteed for 1 year from date of receipt.

Publications for Transgelin/TAGLN/SM22 alpha Antibody (NBP1-33003)(4)

Publications using NBP1-33003

• Cao T, Jiang Y, Li D et al. H19/TET1 axis promotes TGF-beta signaling linked to endothelial-to-mesenchymal transition FASEB J. 2020-05-06 [PMID: 32374060]
• Gao R, Kanasaki K, Li J et al. Beta klotho is essential for the anti-endothelial mesenchymal transition effects of N-acetyl-seryl-aspartyl-lysyl-proline FEBS Open Bio. [PMID: 30972974] (WB, Human)
• Li J, Shi S, et al. FGFR1 is critical for the anti-endothelial mesenchymal transition effect of N-acetyl-seryl-aspartyl-lysyl-proline via induction of the MAP4K4 pathway. Cell Death Dis 2017-08-03 [PMID: 28771231] (WB, Mouse)
• Shi S, Srivastava SP, Kanasaki M et al. Interactions of DPP-4 and integrin beta1 influences endothelial-to-mesenchymal transition Kidney Int. 2015-04-01 [PMID: 25830763] (WB, Human)

Bioinformatics

• Gene Symbol: TAGLN
• Entrez:
  • 6876(Human)
• Uniprot:
  • Q01995()