AFfirm™ IL1 beta Mouse Monoclonal Antibody - #BF8021

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Product: IL1 beta Mouse Monoclonal Antibody
Catalog: BF8021
Description: Mouse monoclonal antibody to IL1 beta
Application: WB IF/ICC
Cited expt.: WB
Reactivity: Human, Mouse
Mol.Wt.: 25~35 kD; 31kD(Calculated).
Uniprot: P01584

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 100ul $280 In stock
 200ul $350 In stock

Lead Time: Same day delivery

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Related Downloads
MSDS
Data Sheet
COA
Protocols
WB Handbook
IHC Protocol
IF/ICC Protocol

Product Info

Source:
Mouse
Application:
WB 1:500-1:3000, IF/ICC 1:100-1:500
*The optimal dilutions should be determined by the end user. For optimal experimental results, antibody reuse is not recommended.
*Tips:

WB: For western blot detection of denatured protein samples. IHC: For immunohistochemical detection of paraffin sections (IHC-p) or frozen sections (IHC-f) of tissue samples. IF/ICC: For immunofluorescence detection of cell samples. ELISA(peptide): For ELISA detection of antigenic peptide.

Reactivity:
Human,Mouse
Clonality:
Monoclonal [AFfirm8021]
Specificity:
IL1 beta Antibody detects endogenous levels of total IL1 beta.
Conjugate:
Unconjugated.
Purification:
The antiserum was purified by peptide affinity chromatography using SulfoLink™ Coupling Resin (Thermo Fisher Scientific).
Storage:
Mouse IgG1 in phosphate buffered saline (without Mg2+ and Ca2+), pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol. Store at -20 °C. Stable for 12 months from date of receipt.
Alias:

Fold/Unfold

Catabolin; H1; IL 1; IL 1 beta; IL-1 beta; IL1 BETA; IL1B; IL1B_HUMAN; IL1F2; Interleukin 1 beta; Interleukin-1 beta; OAF; OTTHUMP00000162031; Preinterleukin 1 beta; Pro interleukin 1 beta;

Immunogens

Immunogen:

A synthesized peptide derived from human IL1 beta.

Uniprot:

P01584(IL1B_HUMAN) >>Visit HPA database.

Gene(ID):
IL1B(3553)
Expression:
P01584 IL1B_HUMAN:

Expressed in activated monocytes/macrophages (at protein level).

Sequence:
MAEVPELASEMMAYYSGNEDDLFFEADGPKQMKCSFQDLDLCPLDGGIQLRISDHHYSKGFRQAASVVVAMDKLRKMLVPCPQTFQENDLSTFFPFIFEEEPIFFDTWDNEAYVHDAPVRSLNCTLRDSQQKSLVMSGPYELKALHLQGQDMEQQVVFSMSFVQGEESNDKIPVALGLKEKNLYLSCVLKDDKPTLQLESVDPKNYPKKKMEKRFVFNKIEINNKLEFESAQFPNWYISTSQAENMPVFLGGTKGGQDITDFTMQFVSS

Research Backgrounds

Function:

Potent proinflammatory cytokine. Initially discovered as the major endogenous pyrogen, induces prostaglandin synthesis, neutrophil influx and activation, T-cell activation and cytokine production, B-cell activation and antibody production, and fibroblast proliferation and collagen production. Promotes Th17 differentiation of T-cells. Synergizes with IL12/interleukin-12 to induce IFNG synthesis from T-helper 1 (Th1) cells.

PTMs:

Activation of the IL1B precursor involves a CASP1-catalyzed proteolytic cleavage. Processing and secretion are temporarily associated.

Subcellular Location:

Cytoplasm>Cytosol. Lysosome. Secreted>Extracellular exosome. Secreted.
Note: The precursor is cytosolic. In response to inflammasome-activating signals, such as ATP for NLRP3 inflammasome or bacterial flagellin for NLRC4 inflammasome, cleaved and secreted. IL1B lacks any known signal sequence and the pathway(s) of its secretion is(are) not yet fully understood (PubMed:24201029). On the basis of experimental results, several unconventional secretion mechanisms have been proposed. 1. Secretion via secretory lysosomes: a fraction of CASP1 and IL1B precursor may be incorporated, by a yet undefined mechanism, into secretory lysosomes that undergo Ca(2+)-dependent exocytosis with release of mature IL1B (PubMed:15192144). 2. Secretory autophagy: IL1B-containing autophagosomes may fuse with endosomes or multivesicular bodies (MVBs) and then merge with the plasma membrane releasing soluble IL1B or IL1B-containing exosomes (PubMed:24201029). However, autophagy impacts IL1B production at several levels and its role in secretion is still controversial. 3. Secretion via exosomes: ATP-activation of P2RX7 leads to the formation of MVBs containing exosomes with entrapped IL1B, CASP1 and other inflammasome components. These MVBs undergo exocytosis with the release of exosomes. The release of soluble IL1B occurs after the lysis of exosome membranes (By similarity). 4. Secretion by microvesicle shedding: activation of the ATP receptor P2RX7 may induce an immediate shedding of membrane-derived microvesicles containing IL1B and possibly inflammasome components. The cytokine is then released in the extracellular compartment after microvesicle lysis (PubMed:11728343). 5. Release by translocation through permeabilized plasma membrane. This may occur in cells undergoing pyroptosis due to sustained activation of the inflammasome (By similarity). These mechanisms may not be not mutually exclusive.

Extracellular region or secreted Cytosol Plasma membrane Cytoskeleton Lysosome Endosome Peroxisome ER Golgi apparatus Nucleus Mitochondrion Manual annotation Automatic computational assertionSubcellular location
Tissue Specificity:

Expressed in activated monocytes/macrophages (at protein level).

Family&Domains:

Belongs to the IL-1 family.

Research Fields

· Cellular Processes > Cell growth and death > Necroptosis.   (View pathway)

· Environmental Information Processing > Signal transduction > MAPK signaling pathway.   (View pathway)

· Environmental Information Processing > Signaling molecules and interaction > Cytokine-cytokine receptor interaction.   (View pathway)

· Environmental Information Processing > Signal transduction > NF-kappa B signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > TNF signaling pathway.   (View pathway)

· Human Diseases > Drug resistance: Antineoplastic > Antifolate resistance.

· Human Diseases > Endocrine and metabolic diseases > Non-alcoholic fatty liver disease (NAFLD).

· Human Diseases > Endocrine and metabolic diseases > Type I diabetes mellitus.

· Human Diseases > Neurodegenerative diseases > Alzheimer's disease.

· Human Diseases > Neurodegenerative diseases > Prion diseases.

· Human Diseases > Infectious diseases: Bacterial > Salmonella infection.

· Human Diseases > Infectious diseases: Bacterial > Pertussis.

· Human Diseases > Infectious diseases: Bacterial > Legionellosis.

· Human Diseases > Infectious diseases: Parasitic > Leishmaniasis.

· Human Diseases > Infectious diseases: Parasitic > Chagas disease (American trypanosomiasis).

· Human Diseases > Infectious diseases: Parasitic > African trypanosomiasis.

· Human Diseases > Infectious diseases: Parasitic > Malaria.

· Human Diseases > Infectious diseases: Parasitic > Amoebiasis.

· Human Diseases > Infectious diseases: Bacterial > Tuberculosis.

· Human Diseases > Infectious diseases: Viral > Measles.

· Human Diseases > Infectious diseases: Viral > Influenza A.

· Human Diseases > Infectious diseases: Viral > Herpes simplex infection.

· Human Diseases > Immune diseases > Inflammatory bowel disease (IBD).

· Human Diseases > Immune diseases > Rheumatoid arthritis.

· Human Diseases > Immune diseases > Graft-versus-host disease.

· Organismal Systems > Development > Osteoclast differentiation.   (View pathway)

· Organismal Systems > Immune system > Toll-like receptor signaling pathway.   (View pathway)

· Organismal Systems > Immune system > NOD-like receptor signaling pathway.   (View pathway)

· Organismal Systems > Immune system > Cytosolic DNA-sensing pathway.   (View pathway)

· Organismal Systems > Immune system > Hematopoietic cell lineage.   (View pathway)

· Organismal Systems > Immune system > IL-17 signaling pathway.   (View pathway)

· Organismal Systems > Immune system > Th17 cell differentiation.   (View pathway)

· Organismal Systems > Sensory system > Inflammatory mediator regulation of TRP channels.   (View pathway)

References

1). Antibiotic cocktail-induced changes in gut microbiota drive alteration of bile acid metabolism to restrain Th17 differentiation through the FXR-NLRP3 axis. Gut microbes, 2025 (PubMed: 41305918) [IF=12.2]

Application: WB    Species: Mouse    Sample:

Figure 6. DCA initiates the NLRP3‒IL17A pathway to promote Th17 differentiation (A) Feeding schedule for EAP mice treated with ABX, ABX + DCA or ABX + DCA + MCC950. (B) Assessment of pelvic pain in mice using von Frey filaments. (C) H&E staining revealing alterations in prostate tissue. The red arrow indicates the invasion of inflammatory cells. Inflammation score assessment in the ABX, ABX + DCA and ABX + DCA + MCC950 groups. (D) Relative level of RORγt mRNA in prostate tissue from ABX, ABX + DCA and ABX + DCA + MCC950 mice. (E, F) The percentages of CD4+ IL-17A + and CD4+ RORγt + cells in the spleen of ABX, ABX + DCA and ABX + DCA + MCC950 mice. (G, H) Sorted naïve CD4+ T cells were activated for 5 days under Th17 cell differentiation conditions without DCA (media group), with DCA (media + DCA group) or with DCA + MCC950 (media + DCA + MCC950 group). Representative images and analysis of FCM staining for CD4+ IL-17A + cells and CD4+ RORγt + cells in the three groups. (I) Western blot analysis of NLRP3-IL17A-related proteins in the media, media + DCA, and media + DCA + MCC950 groups (n = 3). (J) IHC of NLRP3-IL17A-related proteins in prostate tissue from ABX, ABX + DCA and ABX + DCA + MCC950 mice. (K) ChIP‒qPCR was used to determine the binding status of FXR at three sites in the NLRP3 promoter. (L) Dual-luciferase assay showing the interaction between FXR and NLRP3. (n = 3–5; *, P 
2). A biomaterial-based therapy using a sodium hyaluronate/bioglass composite hydrogel for the treatment of oral submucous fibrosis. Acta Biomaterialia, 2023 (PubMed: 36509401) [IF=9.4]
3). Multi-omics analysis identified and confirmed TNF-α as a key initiator of the inflammatory response following spinal cord injury. International journal of biological macromolecules, 2025 (PubMed: 40319972) [IF=7.7]
4). Sophora moocroftiana seeds ethanol extract regulates NLRP3 inflammasome activation and pyroptosis via ROS/TXNIP pathway to amelioration of NAFLD in vitro and in vivo. Frontiers in pharmacology, 2025 (PubMed: 40926986) [IF=5.6]

Application: IHC    Species: Mouse    Sample:

Figure 5. Effect of SMS on TXNIP/NLRP3 pathway of pyroptosis in HFD-fed C57BL/6J mice. Snap frozen liver tissue sections of mice were analyzed by IHC for TXNIP, NLRP3, GSDMD and IL-1β and a representative image of mice per group has been displayed (200×). Silymarin (100 mg/kg) was used as the positive control.
5). HCMV-IE2 promotes atherosclerosis by inhibiting vascular smooth muscle cells' pyroptosis. Frontiers in microbiology, 2023 (PubMed: 37234524) [IF=5.2]
6). Demethyleneberberine blocked the maturation of IL-1β in inflammation by inhibiting TLR4-mitochondria signaling. International Immunopharmacology, 2022 (PubMed: 36252484) [IF=4.8]
7). An integrated approach of experiment validation and single-cell RNA sequencing reveal dual-pathway inhibition of NLRP3/ferroptosis by flavonoids of Sanyeqing fibrous root in acute lung injury. Journal of ethnopharmacology, 2026 (PubMed: 41115482) [IF=4.8]

Application: WB    Species: Mouse    Sample:

Fig. 6. Effects of SYQfr-F on NLRP3 inflammasome expression in LPS-Induced ALI in vivo and in vitro. Western blot analysis of NLRP3, IL-1β, ASC, IL-18, and cleaved-caspase-1 protein expression in LPS-induced ALI in vivo (A–F). qRT-PCR analysis of NLRP3, IL-1β, ASC, IL-18, and caspase-1 mRNA expression in LPS-induced ALI in vivo (G–K). Western blot analysis of NLRP3, IL-1β, and ASC protein expression in LPS-induced ALI in vitro (L–O). (R–S) Immunofluorescence staining of NLRP3 and ASC in LPS-induced ALI in vitro. Fluorescence intensity analysis of ASC and cleaved-caspase-1 in LPS-induced ALI in vitro (P–Q).
8). RBPMS2 can inhibit the NLRP3 / caspase-1 / GSDMD signaling pathway to resist pyroptosis in gastric cancer cells. Scientific reports, 2025 (PubMed: 40595708) [IF=3.8]
9). Ascorbic acid relieves neuropathic pain and depressive behavior by reducing inflammation and activating antioxidant responses. Molecular pain, 2025 (PubMed: 40616463) [IF=3.3]
10). Ursolic acid alleviates liver injury in diabetic mice induced by high-fat diet combined with streptozotocin via the NLRP3 signaling pathway. PloS one, 2026 (PubMed: 41637437) [IF=2.9]
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