IL-1 beta/IL-1F2 Antibody [Unconjugated]

Recombinant Mouse IL‑1 beta /IL‑1F2 (Catalog # 401-ML) stimulates proliferation in the the D10.G4.1 mouse helper T cell line in a dose-dependent manner (orange line). Proliferation elicited by Recombinant Mouse IL‑1 beta /IL‑1F2 (10 pg/mL) is neutralized (green line) by increasing concentrations of Goat Anti-Mouse IL‑1 beta /IL‑1F2 Polyclonal Antibody (Catalog # AB-401-NA). The ND50 is typically 2-12 µg/mL.

Western blot shows lysates of THP-1 human acute monocytic leukemia cell line untreated (-) or treated (+) with 200 nM PMA for 24 hours and 10 µg/mL LPS for 4 hours and RAW 264.7 mouse monocyte/macrophage cell line untreated (-) or treated (+) with 10 µg/mL LPS for 24 hours. PVDF membrane was probed with 1 µg/mL of Goat Anti-Mouse IL-1 beta /IL-1F2 Polyclonal Antibody (Catalog # AB-401-NA) followed by HRP-conjugated Anti-Goat IgG Secondary Antibody (HAF017). A specific band was detected for IL-1 beta /IL-1F2 at approximately 35 kDa (as indicated). This experiment was conducted under reducing conditions and using Immunoblot Buffer Group 1.

Simple Western lane view shows lysates of RAW 264.7 mouse monocyte/macrophage cell line untreated (-) or treated (+) with 10 µg/mL LPS for 24 hours, loaded at 0.5 mg/mL. A specific band was detected for IL‑1 beta /IL‑1F2 at approximately 40 kDa (as indicated) using 50 µg/mL of Goat Anti-Mouse IL‑1 beta /IL‑1F2 Polyclonal Antibody (Catalog # AB-401-NA) . This experiment was conducted under reducing conditions and using the12-230 kDa separation system.

GlcN inhibits caspase-1 activation and the release of IL-1 beta , IL-18 and ASC. (A–D) J774A.1 macrophages were incubated for 4 h with LPS (1 µg/ml) followed by incubation for 2 h with GlcN. Cells were then incubated with ATP (5 mM, 0.5 h) or infected with E. coli (30 MOI, 1 h). The expression levels of IL-1 beta and IL-18 (A), caspase-1 (C), ASC (D) in the supernatants and IL-1 beta in the cell lysates (B) were analysed by Western blotting. (E) J774A.1 macrophages were incubated for 4 h with LPS (1 µg/ml) followed by incubation for 2 h with GlcN, D-(+)-glucose (Glu), D-glucosamine 3-sulphate (GlcN-3S), D-(+)-galactosamine hydrochloride (GalN) and N-acetyl-D-glucosamine (GlcNAc) for 2 h, followed by incubation with ATP (5 mM) for 0.5 h. The IL-1 beta expression levels in the supernatants were measured by ELISA. (F) J774A.1 macrophages were incubated for 4 h with LPS (1 µg/ml) or PamsCSK4 (1 µg/ml; for non-canonical inflammasome) followed by incubation for 2 h with GlcN, followed by transfection with poly(dA/dT) (2 µg/ml) or LPS (2 µg/ml) for 6 h or by Salmonella infection (30 MOI) for 2 h. The IL-1 beta expression levels in the supernatants were measured by ELISA. The ELISA data are expressed as the mean ± SD of separate experiments as indicated. The Western blotting results are representative of three different experiments and the histogram shows the quantification expressed as the mean ± SD for these three experiments. *, *** and **** indicate a significant difference at the level of p < 0.05, p < 0.001 and p < 0.0001, respectively, compared to NLRP3 activator-treated cells. (One-way ANOVA with Dunnett’s multiple comparisons test). The blots in (A–D) were cropped from different gels; full-length blots are included in the “Supplementary Information”. Image collected and cropped by CiteAb from the following open publication (//pubmed.ncbi.nlm.nih.gov/30944389), licensed under a CC-BY license. Not internally tested by R&D Systems.

CVL reduced NLRP3 inflammasome activation. (A) J774A.1 macrophages were incubated for 5 h with LPS (1 μg/ml) (LPS priming) followed by incubation for 0.5 h with CVL. Cells were then incubated with CC (100 μg/ml, 24 h), MSU (100 μg/ml, 24 h), ATP (5 mM, 0.5 h), nigericin (10 μM, 0.5 h), and nano-SiO2 (100 μg/ml, 24 h). (B) LPS-primed J774A.1 macrophages were incubated for 0.5 h with CVL followed by incubation with CC (100 μg/ml, 24 h), MSU (100 μg/ml, 24 h), and ATP (5 mM, 0.5 h). (C) LPS-primed BMDM were incubated for 0.5 h with CVL followed by incubation with CC (100 μg/ml) for an additional 24 h. (D) LPS-primed or Pam3CSK4-primed (for LPS transfection only) cells were incubated for 0.5 h with CVL followed by transfection with poly(dA/dT) (2 μg/ml, 6 h), FLA-ST (1 μg/ml, 6 h), MDP (10 μg/ml, 6 h), or LPS (2 μg/ml, 6 h). The levels of IL-1 beta , IL-18, NLRP3, ASC, and caspase-1 in the culture medium were measured by Western blot. The IL-1 beta levels in the supernatants were measured by ELISA. The Western blot results are representative of three different experiments. The ELISA data are expressed as the mean ± SD of three separate experiments. *, **, and *** indicate a significant difference at the level of p < 0.05, p < 0.01, and p < 0.001, respectively, compared to activator-treated cells. Image collected and cropped by CiteAb from the following open publication (//pubmed.ncbi.nlm.nih.gov/30186288), licensed under a CC-BY license. Not internally tested by R&D Systems.

F240B inhibits the NLRP3 inflammasome through autophagy induction. (A, B) J774A.1 macrophages were incubated with 1 µg/ml LPS for 5 h followed by incubated with F240B for 3 h. Cells then incubated with 5 mM ATP for 0.5 h. The levels of IL-1 beta and caspase-1 (A) or NLRP3 and ASC (B) in the supernatants were measured by Western blotting. (C) J774A.1 macrophages were incubated with 1 µg/ml LPS for 5 h followed by incubated with 1 µM F240B in the presence or absence of 5 mM 3-MA for 3 h. Cells then were incubated with 5 mM ATP or 10 μM nigericin for 0.5 h. The levels of IL-1 beta in the supernatants were measured by ELISA. (D) Wild-type and LC3-knockout J774A.1 macrophages were incubated with 1 µg/ml LPS for 5 h followed by incubated with 1 µM F240B for 3 h. Cells then incubated with 5 mM ATP or 10 μM nigericin for 0.5 h. The levels of IL-1 beta in the supernatants were measured by ELISA. The data are expressed as the mean ± SD of three separate experiments. * and *** indicate a significant difference at the level of p < 0.05 and p < 0.001, respectively. Image collected and cropped by CiteAb from the following open publication (//pubmed.ncbi.nlm.nih.gov/33424855), licensed under a CC-BY license. Not internally tested by R&D Systems.

ALKBH5 regulates the expression of innate immune response genes during bacterial and viral infections in RAW264.7 cells. (A) ALKBH5 knockdown enhanced the expression levels of the IL-1 beta , CSF3, TGM2, and SRC transcripts during P. aeruginosa, C. diphtheriae, HSV-1, or HSV-1 ICP34.5 mutant infection. (B to D) ALKBH5 knockdown enhanced the protein level of IL-1 beta during infection by C. diphtheriae (B), P. aeruginosa (C), or the HSV-1 ICP34.5 mutant (D). (E) ALKBH5 overexpression inhibited the expression of the IL-1 beta , CSF3, TGM2, and SRC genes during P. aeruginosa infection as measured by RT-qPCR. (F) ALKBH5 overexpression inhibited the protein level of IL-1 beta during P. aeruginosa infection as measured by Western blotting. Image collected and cropped by CiteAb from the following open publication (//pubmed.ncbi.nlm.nih.gov/36625590), licensed under a CC-BY license. Not internally tested by R&D Systems.

DUSP1 regulates p38 and JNK phosphorylation and the expression of innate immune response genes during bacterial and viral infections in RAW264.7 cells. (A) DUSP1 knockdown enhanced p38 and JNK phosphorylation during infection by P. aeruginosa, C. diphtheriae, HSV-1, or the HSV-1 ICP34.5 mutant. (B) DUSP1 knockdown enhanced the expression of the IL-1 beta , CSF3, TGM2, and SRC genes during infection by P. aeruginosa, C. diphtheriae, HSV-1, or the HSV-1 ICP34.5 mutant. (C) DUSP1 knockdown enhanced the protein level of IL-1 beta during infection by P. aeruginosa, C. diphtheriae, or the HSV-1 ICP34.5 mutant. Image collected and cropped by CiteAb from the following open publication (//pubmed.ncbi.nlm.nih.gov/36625590), licensed under a CC-BY license. Not internally tested by R&D Systems.

ALKBH5 regulates the expression of innate immune response genes during bacterial and viral infections in RAW264.7 cells. (A) ALKBH5 knockdown enhanced the expression levels of the IL-1 beta , CSF3, TGM2, and SRC transcripts during P. aeruginosa, C. diphtheriae, HSV-1, or HSV-1 ICP34.5 mutant infection. (B to D) ALKBH5 knockdown enhanced the protein level of IL-1 beta during infection by C. diphtheriae (B), P. aeruginosa (C), or the HSV-1 ICP34.5 mutant (D). (E) ALKBH5 overexpression inhibited the expression of the IL-1 beta , CSF3, TGM2, and SRC genes during P. aeruginosa infection as measured by RT-qPCR. (F) ALKBH5 overexpression inhibited the protein level of IL-1 beta during P. aeruginosa infection as measured by Western blotting. Image collected and cropped by CiteAb from the following open publication (//pubmed.ncbi.nlm.nih.gov/36625590), licensed under a CC-BY license. Not internally tested by R&D Systems.

ALKBH5 regulates the expression of innate immune response genes during bacterial and viral infections in RAW264.7 cells. (A) ALKBH5 knockdown enhanced the expression levels of the IL-1 beta , CSF3, TGM2, and SRC transcripts during P. aeruginosa, C. diphtheriae, HSV-1, or HSV-1 ICP34.5 mutant infection. (B to D) ALKBH5 knockdown enhanced the protein level of IL-1 beta during infection by C. diphtheriae (B), P. aeruginosa (C), or the HSV-1 ICP34.5 mutant (D). (E) ALKBH5 overexpression inhibited the expression of the IL-1 beta , CSF3, TGM2, and SRC genes during P. aeruginosa infection as measured by RT-qPCR. (F) ALKBH5 overexpression inhibited the protein level of IL-1 beta during P. aeruginosa infection as measured by Western blotting. Image collected and cropped by CiteAb from the following open publication (//pubmed.ncbi.nlm.nih.gov/36625590), licensed under a CC-BY license. Not internally tested by R&D Systems.

DUSP1 regulates p38 and JNK phosphorylation and the expression of innate immune response genes during bacterial and viral infections in RAW264.7 cells. (A) DUSP1 knockdown enhanced p38 and JNK phosphorylation during infection by P. aeruginosa, C. diphtheriae, HSV-1, or the HSV-1 ICP34.5 mutant. (B) DUSP1 knockdown enhanced the expression of the IL-1 beta , CSF3, TGM2, and SRC genes during infection by P. aeruginosa, C. diphtheriae, HSV-1, or the HSV-1 ICP34.5 mutant. (C) DUSP1 knockdown enhanced the protein level of IL-1 beta during infection by P. aeruginosa, C. diphtheriae, or the HSV-1 ICP34.5 mutant. Image collected and cropped by CiteAb from the following open publication (//pubmed.ncbi.nlm.nih.gov/36625590), licensed under a CC-BY license. Not internally tested by R&D Systems.

CS inhibits NLRP3 inflammasome activation. (A–D) J774A.1 macrophages were primed with LPS for 5 h and incubated with CS for 0.5 h Cells were stimulated with 10 μM nigericin for 0.5 h The levels of IL-1 beta in the supernatants were measured by ELISA (A) and Western blot (B). The levels of IL-18 (C) and caspase-1 (D) in the supernatants were measured by Western blot. (E, F) Human THP-1 macrophages or PBMC were primed with LPS for 5 h and incubated with CS for 0.5 h Cells were stimulated with 10 μM nigericin for 0.5 h The levels of IL-1 beta in the supernatants were measured by ELISA. (G, H) J774A.1 macrophages were primed with LPS for 5 h and incubated with CS for 0.5 h Cells were stimulated with 5 mM ATP for 0.5 h The levels of IL-1 beta in the supernatants were measured by ELISA (G) and the levels of caspase-1 in the supernatants were measured by Western blot (H). (I) J774A.1 macrophages were primed with LPS or Pam3CSK4 (for non-canonical inflammasome) for 5 h and incubated with CS for 0.5 h Cells were transfected with poly(dA/dT), LPS, MDP or FLA-ST for 6 h or infected with Salmonella for 2 h The levels of IL-1 beta in the supernatants were measured by ELISA. (J) J774A.1 macrophages were primed with LPS for 5 h and incubated with Irbesartan (IS) for 0.5 h Cells were stimulated with 10 μM nigericin for 0.5 h The levels of IL-1 beta in the supernatants were measured by ELISA. The ELISA data are expressed as the means ± SD of the three separate experiments. The Western blot images are representative results, and the histogram shows the band intensity. *, ** and *** indicate a significant difference at the level of p<0.05, p<0.01 and p<0.001, respectively, compared to nigericin- or ATP-activated cells or as indicated. Image collected and cropped by CiteAb from the following open publication (//pubmed.ncbi.nlm.nih.gov/35669789), licensed under a CC-BY license. Not internally tested by R&D Systems.

ALKBH5 regulates the expression of innate immune response genes during bacterial and viral infections in RAW264.7 cells. (A) ALKBH5 knockdown enhanced the expression levels of the IL-1 beta , CSF3, TGM2, and SRC transcripts during P. aeruginosa, C. diphtheriae, HSV-1, or HSV-1 ICP34.5 mutant infection. (B to D) ALKBH5 knockdown enhanced the protein level of IL-1 beta during infection by C. diphtheriae (B), P. aeruginosa (C), or the HSV-1 ICP34.5 mutant (D). (E) ALKBH5 overexpression inhibited the expression of the IL-1 beta , CSF3, TGM2, and SRC genes during P. aeruginosa infection as measured by RT-qPCR. (F) ALKBH5 overexpression inhibited the protein level of IL-1 beta during P. aeruginosa infection as measured by Western blotting. Image collected and cropped by CiteAb from the following open publication (//pubmed.ncbi.nlm.nih.gov/36625590), licensed under a CC-BY license. Not internally tested by R&D Systems.

ALKBH5 regulates the expression of innate immune response genes during bacterial and viral infections in RAW264.7 cells. (A) ALKBH5 knockdown enhanced the expression levels of the IL-1 beta , CSF3, TGM2, and SRC transcripts during P. aeruginosa, C. diphtheriae, HSV-1, or HSV-1 ICP34.5 mutant infection. (B to D) ALKBH5 knockdown enhanced the protein level of IL-1 beta during infection by C. diphtheriae (B), P. aeruginosa (C), or the HSV-1 ICP34.5 mutant (D). (E) ALKBH5 overexpression inhibited the expression of the IL-1 beta , CSF3, TGM2, and SRC genes during P. aeruginosa infection as measured by RT-qPCR. (F) ALKBH5 overexpression inhibited the protein level of IL-1 beta during P. aeruginosa infection as measured by Western blotting. Image collected and cropped by CiteAb from the following open publication (//pubmed.ncbi.nlm.nih.gov/36625590), licensed under a CC-BY license. Not internally tested by R&D Systems.

CS inhibits NLRP3 inflammasome activation. (A–D) J774A.1 macrophages were primed with LPS for 5 h and incubated with CS for 0.5 h Cells were stimulated with 10 μM nigericin for 0.5 h The levels of IL-1 beta in the supernatants were measured by ELISA (A) and Western blot (B). The levels of IL-18 (C) and caspase-1 (D) in the supernatants were measured by Western blot. (E, F) Human THP-1 macrophages or PBMC were primed with LPS for 5 h and incubated with CS for 0.5 h Cells were stimulated with 10 μM nigericin for 0.5 h The levels of IL-1 beta in the supernatants were measured by ELISA. (G, H) J774A.1 macrophages were primed with LPS for 5 h and incubated with CS for 0.5 h Cells were stimulated with 5 mM ATP for 0.5 h The levels of IL-1 beta in the supernatants were measured by ELISA (G) and the levels of caspase-1 in the supernatants were measured by Western blot (H). (I) J774A.1 macrophages were primed with LPS or Pam3CSK4 (for non-canonical inflammasome) for 5 h and incubated with CS for 0.5 h Cells were transfected with poly(dA/dT), LPS, MDP or FLA-ST for 6 h or infected with Salmonella for 2 h The levels of IL-1 beta in the supernatants were measured by ELISA. (J) J774A.1 macrophages were primed with LPS for 5 h and incubated with Irbesartan (IS) for 0.5 h Cells were stimulated with 10 μM nigericin for 0.5 h The levels of IL-1 beta in the supernatants were measured by ELISA. The ELISA data are expressed as the means ± SD of the three separate experiments. The Western blot images are representative results, and the histogram shows the band intensity. *, ** and *** indicate a significant difference at the level of p<0.05, p<0.01 and p<0.001, respectively, compared to nigericin- or ATP-activated cells or as indicated. Image collected and cropped by CiteAb from the following open publication (//pubmed.ncbi.nlm.nih.gov/35669789), licensed under a CC-BY license. Not internally tested by R&D Systems.

ALKBH5 regulates the expression of innate immune response genes during bacterial and viral infections in RAW264.7 cells. (A) ALKBH5 knockdown enhanced the expression levels of the IL-1 beta , CSF3, TGM2, and SRC transcripts during P. aeruginosa, C. diphtheriae, HSV-1, or HSV-1 ICP34.5 mutant infection. (B to D) ALKBH5 knockdown enhanced the protein level of IL-1 beta during infection by C. diphtheriae (B), P. aeruginosa (C), or the HSV-1 ICP34.5 mutant (D). (E) ALKBH5 overexpression inhibited the expression of the IL-1 beta , CSF3, TGM2, and SRC genes during P. aeruginosa infection as measured by RT-qPCR. (F) ALKBH5 overexpression inhibited the protein level of IL-1 beta during P. aeruginosa infection as measured by Western blotting. Image collected and cropped by CiteAb from the following open publication (//pubmed.ncbi.nlm.nih.gov/36625590), licensed under a CC-BY license. Not internally tested by R&D Systems.

• Reactivity: Mu
• Applications: WB, Simple Western, B/N
• Clonality: Polyclonal
• Host: Goat
• Conjugate: Unconjugated
• Concentration: LYOPH

IL-1 beta/IL-1F2 Antibody [Unconjugated] Summary

• Immunogen: E. coli-derived recombinant mouse IL-1 beta /IL-1F2
  Val118-Ser269
  Accession # P10749
• Specificity: Detects mouse IL-1 beta /IL-1F2 in direct ELISAs and Western blots. In direct ELISAs, approximately 40% cross-reactivity with recombinant cotton rat IL-1 beta and recombinant rhesus monkey IL-1 beta is observed, approximately 15% cross-reactivity with recombinant rat IL-1 beta and recombinant rabbit IL-1 beta is observed, and less than 10% cross-reactivity with recombinant canine IL-1 beta , recombinant equine IL-1 beta , recombinant guinea pig IL-1 beta , recombinant porcine IL-1 beta , recombinant feline IL-1 beta , and recombinant human IL-1 beta is observed.
• Source: N/A
• Isotype: IgG
• Clonality: Polyclonal
• Host: Goat
• Gene: IL1B
• Purity Statement: Protein A or G purified
• Endotoxin Note: <0.10 EU per 1 μg of the antibody by the LAL method.

Applications/Dilutions

• Dilutions:
  • Neutralization 2-12 ug/mL
  • Simple Western 50 ug/mL
  • Western Blot 1 ug/mL

Packaging, Storage & Formulations

• Storage: Use a manual defrost freezer and avoid repeated freeze-thaw cycles.
  • 12 months from date of receipt, -20 to -70 °C as supplied.
  • 1 month, 2 to 8 °C under sterile conditions after reconstitution.
  • 6 months, -20 to -70 °C under sterile conditions after reconstitution.
• Buffer: Lyophilized from a 0.2 μm filtered solution in PBS with Trehalose.
• Preservative: No Preservative
• Concentration: LYOPH
• Reconstitution Instructions: Reconstitute at 1 mg/mL in sterile PBS.

Notes

This product is produced by and ships from R&D Systems, Inc., a Bio-Techne brand.

Alternate Names for IL-1 beta/IL-1F2 Antibody [Unconjugated]

• Catabolin
• IL1 beta
• IL-1 beta
• IL-1
• IL1B
• IL-1b
• IL1-BETA
• IL-1F2
• IL1F2IL-1 beta
• interleukin 1, beta
• interleukin-1 beta
• preinterleukin 1 beta
• pro-interleukin-1-beta

Background

IL-1 is a name that designates two pleiotropic cytokines, IL-1 alpha (IL-1F1) and IL-1 beta (IL-1F2, IL1B), which are the products of distinct genes. IL-1 alpha and IL-1 beta are structurally related polypeptides that share approximately 17% amino acid (aa) identity in mouse. Both proteins are produced by a wide variety of cells in response to inflammatory agents, infections, or microbial endotoxins. While IL-1 alpha and IL-1 beta are regulated independently, they bind to the same receptor and exert identical biological effects. IL-1 RI binds directly to IL-1 alpha or IL-1 beta and then associates with IL-1 R accessory protein (IL-1 R3/IL-1 R AcP) to form a high-affinity receptor complex that is competent for signal transduction. IL-1 RII has high affinity for IL-1 beta but functions as a decoy receptor and negative regulator of IL-1 beta activity. IL-1ra functions as a competitive antagonist by preventing IL-1 alpha and IL-1 beta from interacting with IL-1 RI. Intracellular cleavage of the IL-1 beta precursor by Caspase-1/ICE is a key step in the inflammatory response. The 17 kDa molecular weight mature mouse IL-1 beta shares 90% aa sequence identity with cotton rat and rat and 67%-78% with canine, equine, feline, human, porcine, and rhesus macaque IL-1 beta . IL-1 beta functions in a central role in immune and inflammatory responses, bone remodeling, fever, carbohydrate metabolism, and GH/IGF-I physiology. IL-1 beta dysregulation is implicated in many pathological conditions including sepsis, rheumatoid arthritis, inflammatory bowel disease, acute and chronic myelogenous leukemia, insulin-dependent diabetes mellitus, atherosclerosis, neuronal injury, and aging-related diseases.

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 IL-1 beta/IL-1F2 Antibody (AB-401-NA)(33)

Publications using AB-401-NA

• Xiao, N;Kogishi, A;Radochonski, L;Lei, Y;Chen, J; Type A cholesterol-dependent cytolysins translocate to the trans-Golgi network for NLRP3 inflammasome activation Nature immunology 2025-09-05 [PMID: 40913097] (Western Blot, Human)
• Lin, WY;Tsui, JL;Chiu, HW;Wong, WT;Wu, CH;Hsu, HT;Ho, CL;Yeh, SP;Rao, YK;Chen, A;Wang, CC;Hsu, CH;Chernikov, OV;Hua, KF;Li, LH; Exploring Candesartan, an angiotensin II receptor antagonist, as a novel inhibitor of NLRP3 inflammasome: alleviating inflammation in Neisseria gonorrhoeae infection BMC infectious diseases 2024-11-22 [PMID: 39578786] (Western Blot, Mouse)
• Zhao, C;Sun, L;Zhang, Y;Shu, X;Hu, Y;Chen, D;Zhang, Z;Xia, S;Yang, H;Bao, X;Li, J;Xu, Y; Thymol improves ischemic brain injury by inhibiting microglia-mediated neuroinflammation Brain research bulletin 2024-07-14 [PMID: 39009094] (Western Blot, Mouse)
• Li, Y;Zhuang, Y;Chen, Y;Wang, G;Tang, Z;Zhong, Y;Zhang, Y;Wu, L;Ji, X;Zhang, Q;Pan, B;Luo, Y; Euphorbia factor L2 alleviated gouty inflammation by specifically suppressing both the priming and activation of NLRP3 inflammasome International immunopharmacology 2024-07-08 [PMID: 38981223] (Western Blot, Mouse)
• J Feng, W Meng, L Chen, X Zhang, A Markazi, W Yuan, Y Huang, SJ Gao N6-Methyladenosine and Reader Protein YTHDF2 Enhance the Innate Immune Response by Mediating DUSP1 mRNA Degradation and Activating Mitogen-Activated Protein Kinases during Bacterial and Viral Infections MBio, 2023-01-10;0(0):e0334922. 2023-01-10 [PMID: 36625590] (Western Blot, Mouse)
• Lin WY, Li LH, Hsiao YY et al. Repositioning of the Angiotensin II Receptor Antagonist Candesartan as an Anti-Inflammatory Agent With NLRP3 Inflammasome Inhibitory Activity Frontiers in Immunology 2022-05-20 [PMID: 35669789]
• Lin WY, Li LH, Hsiao YY et al. Repositioning of the Angiotensin II Receptor Antagonist Candesartan as an Anti-Inflammatory Agent With NLRP3 Inflammasome Inhibitory Activity Frontiers in Immunology 5/20/2022 [PMID: 35669789]
• S Arumugam, Y Qin, Z Liang, SN Han, SLT Boodapati, J Li, Q Lu, RA Flavell, WZ Mehal, X Ouyang GSK3beta mediates the spatiotemporal dynamics of NLRP3 inflammasome activation Cell Death and Differentiation, 2022-04-27;0(0):. 2022-04-27 [PMID: 35477991] (Western Blot, Mouse)
• X Ding, H Kambara, R Guo, A Kanneganti, M Acosta-Zal, J Li, F Liu, T Bei, W Qi, X Xie, W Han, N Liu, C Zhang, X Zhang, H Yu, L Zhao, F Ma, JR Köhler, HR Luo Inflammasome-mediated GSDMD activation facilitates escape of Candida albicans from macrophages Nature Communications, 2021-11-18;12(1):6699. 11/18/2021 [PMID: 34795266]
• GM Childers, CA Perry, B Blachut, N Martin, CD Bortner, S Sieber, JL Li, MB Fessler, GJ Harry Assessing the Association of Mitochondrial Function and Inflammasome Activation in Murine Macrophages Exposed to Select Mitotoxic Tri-Organotin Compounds Environmental health perspectives, 2021-04-30;129(4):47015. 2021-04-30 [PMID: 33929904] (Western Blot, Mouse)
• Wu CH, Gan CH, Li LH et al. A Synthetic Small Molecule F240B Decreases NLRP3 Inflammasome Activation by Autophagy Induction Frontiers in Immunology 12/18/2020 [PMID: 33424855]
• Wu CH, Gan CH, Li LH et al. A Synthetic Small Molecule F240B Decreases NLRP3 Inflammasome Activation by Autophagy Induction Frontiers in Immunology 2020-12-18 [PMID: 33424855]
• K Sato, A Tobo, C Mogi, M Tobo, N Yamane, M Tosaka, H Tomura, DS Im, F Okajima The protective role of proton-sensing TDAG8 in the brain injury in a mouse ischemia reperfusion model Sci Rep, 2020-10-14;10(1):17193. 2020-10-14 [PMID: 33057165] (Western Blot, Mouse)
• Hamida Saleh, Atef M. K. Nassar, Ahmed E. Noreldin, Dalia Samak, Norhan Elshony, Lamiaa Wasef et al. Chemo-Protective Potential of Cerium Oxide Nanoparticles against Fipronil-Induced Oxidative Stress, Apoptosis, Inflammation and Reproductive Dysfunction in Male White Albino Rats Molecules 2020-07-31 [PMID: 32751827] (Immunohistochemistry, Rat)
• Hamida Saleh, Atef M. K. Nassar, Ahmed E. Noreldin, Dalia Samak, Norhan Elshony, Lamiaa Wasef et al. Chemo-Protective Potential of Cerium Oxide Nanoparticles against Fipronil-Induced Oxidative Stress, Apoptosis, Inflammation and Reproductive Dysfunction in Male White Albino Rats Molecules 7/31/2020 [PMID: 32751827]
• Lan-Hui Li, Tzu-Ling Chen, Hsiao-Wen Chiu, Chung-Hua Hsu, Chien-Chun Wang, Tzu-Ting Tai et al. Critical Role for the NLRP3 Inflammasome in Mediating IL-1 beta Production in Shigella sonnei-Infected Macrophages Frontiers in Immunology 6/3/2020 [PMID: 32582195]
• YH Jeong, MC Walsh, J Yu, H Shen, EJ Wherry, Y Choi Mice Lacking the Purinergic Receptor P2X5 Exhibit Defective Inflammasome Activation and Early Susceptibility to Listeria monocytogenes J. Immunol., 2020-06-15;0(0):. 2020-06-15 [PMID: 32540996] (Western Blot, Mouse)
• Hsiao-Wen Chiu, Lan-Hui Li, Chih-Yu Hsieh, Yerra Koteswara Rao, Fang-Hsin Chen, Ann Chen et al. Glucosamine inhibits IL-1 beta expression by preserving mitochondrial integrity and disrupting assembly of the NLRP3 inflammasome Scientific Reports 4/3/2019 [PMID: 30944389]
• H Nakazawa, K Ikeda, S Shinozaki, S Yasuhara, YM Yu, JAJ Martyn, RG Tompkins, T Yorozu, S Inoue, M Kaneki Coenzyme Q10 protects against burn-induced mitochondrial dysfunction and impaired insulin signaling in mouse skeletal muscle FEBS Open Bio, 2019-01-19;9(2):348-363. 2019-01-19 [PMID: 30761259] (Western Blot, Mouse)
• J Chen, ZJ Chen PtdIns4P on dispersed trans-Golgi network mediates NLRP3 inflammasome activation Nature, 2018-11-28;564(7734):71-76. 2018-11-28 [PMID: 30487600] (Western Blot, Mouse)
• Wong WT, Li LH, Rao YK et al. Repositioning of the B-Blocker Carvedilol as a Novel Autophagy Inducer That Inhibits the NLRP3 Inflammasome. Front Immunol 8/22/2018 [PMID: 30186288]
• Xiaoli Tian, He Sun, Amy-Jo Casbon, Edward Lim, Kevin P. Francis, Judith Hellman et al. NLRP3 Inflammasome Mediates Dormant Neutrophil Recruitment following Sterile Lung Injury and Protects against Subsequent Bacterial Pneumonia in Mice Frontiers in Immunology 10/31/2017 [PMID: 29163464]
• Karen V. Swanson, Robert D. Junkins, Cathryn J. Kurkjian, Elizabeth Holley-Guthrie, Avani A. Pendse, Rachid El Morabiti et al. A noncanonical function of cGAMP in inflammasome priming and activation Journal of Experimental Medicine 12/4/2017 [PMID: 29030458]
• Wang H, Hong L, Huang J, Jiang Q, Tao R, Tan C, Lu N, Wang C, Ahmed M, Lu Y, Liu Z, Shi W, Lai E, Wilcox C, Han F P2RX7 sensitizes Mac-1/ICAM-1-dependent leukocyte-endothelial adhesion and promotes neurovascular injury during septic encephalopathy. Cell Res, 2015-05-22;25(6):674-90. 2015-05-22 [PMID: 25998681] (Neutralization, Mouse)
• Coll R, Robertson A, Chae J, Higgins S, Munoz-Planillo R, Inserra M, Vetter I, Dungan L, Monks B, Stutz A, Croker D, Butler M, Haneklaus M, Sutton C, Nunez G, Latz E, Kastner D, Mills K, Masters S, Schroder K, Cooper M, O'Neill L A small-molecule inhibitor of the NLRP3 inflammasome for the treatment of inflammatory diseases. Nat Med, 2015-02-16;21(3):248-55. 2015-02-16 [PMID: 25686105] (Western Blot, Mouse)
• Zhao Y, Xiao X, Frank S, Lin H, Xia Y Distinct mechanisms of induction of hepatic growth hormone resistance by endogenous IL-6, TNF-alpha, and IL-1beta. Am J Physiol Endocrinol Metab, 2014-06-03;307(2):E186-98. 2014-06-03 [PMID: 24895283] (Neutralization, Mouse)
• Sonia Lacroix-Lamandé, Martine Fanton Fanton d’Andon, Eric Michel, Gwenn Ratet, Dana J. Philpott, Stephen E. Girardin et al. Downregulation of the Na/K-ATPase Pump by Leptospiral Glycolipoprotein Activates the NLRP3 Inflammasome The Journal of Immunology 3/15/2012 [PMID: 22323544]
• Sonia Lacroix-Lamandé, Martine Fanton Fanton d’Andon, Eric Michel, Gwenn Ratet, Dana J. Philpott, Stephen E. Girardin et al. Downregulation of the Na/K-ATPase Pump by Leptospiral Glycolipoprotein Activates the NLRP3 Inflammasome The Journal of Immunology 2012-03-15 [PMID: 22323544] (Western Blot, Mouse)
• Chong-Shan Shi, Kevin Shenderov, Ning-Na Huang, Juraj Kabat, Mones Abu-Asab, Katherine A. Fitzgerald et al. Activation of autophagy by inflammatory signals limits IL-1 beta production by targeting ubiquitinated inflammasomes for destruction Nature Immunology 3/1/2012 [PMID: 22286270]
• Reed JR, Leon RP, Hall MK, Schwertfeger KL Interleukin-1beta and fibroblast growth factor receptor 1 cooperate to induce cyclooxygenase-2 during early mammary tumourigenesis. Breast Cancer Res., 2009-04-24;11(2):R21. 2009-04-24 [PMID: 19393083] (Neutralization, Mouse)
• Taki N, Tatro JM, Lowe R, Goldberg VM, Greenfield EM Comparison of the roles of IL-1, IL-6, and TNFalpha in cell culture and murine models of aseptic loosening. Bone, 2006-12-21;40(5):1276-83. 2006-12-21 [PMID: 17236833] (Neutralization, Mouse)
• Shchors K, Shchors E, Rostker F, Lawlor ER, Brown-Swigart L, Evan GI The Myc-dependent angiogenic switch in tumors is mediated by interleukin 1beta. Genes Dev., 2006-09-15;20(18):2527-38. 2006-09-15 [PMID: 16980582] (Neutralization, Mouse)

Bioinformatics

• Gene Symbol: IL1B
• Uniprot:
  • P10749()