产品: Cleaved-IL-1 beta (Asp116) 抗体
货号: AF4006
描述: Rabbit polyclonal antibody to Cleaved-IL-1 beta (Asp116)
反应: Human, Mouse, Rat, Zebrafish
分子量: 17 kDa; 31kD(Calculated).
蛋白号: P01584
RRID: AB_2801567


   规格 价格 库存
 50ul RMB¥ 1250 现货
 100ul RMB¥ 2300 现货
 200ul RMB¥ 3000 现货

货期: 当天发货



WB 1:500-1:2000, IHC 1:50-1:200, IF/ICC 1:100-1:500
*The optimal dilutions should be determined by the end user.

WB: 适用于变性蛋白样本的免疫印迹检测. IHC: 适用于组织样本的石蜡(IHC-p)或冰冻(IHC-f)切片样本的免疫组化/荧光检测. IF/ICC: 适用于细胞样本的荧光检测. ELISA(peptide): 适用于抗原肽的ELISA检测.

Cleaved-IL-1 beta (Asp116) Antibody detects endogenous levels of fragment of activated IL-1 beta resulting from cleavage adjacent to Asp116.
引用格式: Affinity Biosciences Cat# AF4006, RRID:AB_2801567.
The antiserum was purified by peptide affinity chromatography using SulfoLink™ Coupling Resin (Thermo Fisher Scientific).
Rabbit IgG in phosphate buffered saline , pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol. Store at -20 °C. Stable for 12 months from date of receipt.


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;


P01584 IL1B_HUMAN:

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


翻译修饰 - P01584 作为底物

Site PTM Type Enzyme
Y140 Phosphorylation
S200 Phosphorylation
S269 Phosphorylation



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.


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


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

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


Monomer. In its precursor form, weakly interacts with full-length MEFV; the mature cytokine does not interact at all. Interacts with integrins ITGAV:ITGBV and ITGA5:ITGB1; integrin-binding is required for IL1B signaling.


Belongs to the IL-1 family.


· 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)


1). Ou W et al. Hypoxic acclimation improves cardiac redox homeostasis and protects heart against ischemia-reperfusion injury through upregulation of O-GlcNAcylation. Redox Biology 2021 Jul;43:101994. (PubMed: 33964586) [IF=11.4]

Application: WB    Species: rat    Sample: heart

Fig. 3. | HA-induced inflammation stimulated protein O-GlcNAcylation in hearts. A, Immunoblot analysis of IL-1β and IL-6 in the Control and HA hearts (n = 9 per group).

2). Bai X et al. Water-extracted Lonicera japonica polysaccharide attenuates allergic rhinitis by regulating NLRP3-IL-17 signaling axis. Carbohydrate Polymers 2022 Dec 1;297:120053. (PubMed: 36184153) [IF=11.2]

3). Zhang LQ et al. DKK3 ameliorates neuropathic pain via inhibiting ASK-1/JNK/p-38-mediated microglia polarization and neuroinflammation. Journal of Neuroinflammation 2022 Jun 3;19(1):129. (PubMed: 35658977) [IF=9.3]

4). Feng Z et al. Mesenchymal stem cells protect against TBI-induced pyroptosis in vivo and in vitro through TSG-6. Cell Communication and Signaling 2022 Aug 18;20(1):125. (PubMed: 35982465) [IF=8.4]

5). Yu S et al. nNovel insights into antidepressant mechanism of Kai Xin San formula: inhibiting NLRP3 inflammasome activation by promoting autophagy. PHYTOMEDICINE 2021 Oct 4;93:153792. (PubMed: 34735906) [IF=7.9]

6). Wang M et al. Shen Shuai Ⅱ Recipe attenuates renal fibrosis in chronic kidney disease by improving hypoxia-induced the imbalance of mitochondrial dynamics via PGC-1α activation. PHYTOMEDICINE 2022 Jan 19;98:153947. (PubMed: 35104767) [IF=7.9]

7). Huang D et al. Astragaloside IV alleviates PM2.5-caused lung toxicity by inhibiting inflammasome‐mediated pyroptosis via NLRP3/caspase-1 axis inhibition in mice. BIOMEDICINE & PHARMACOTHERAPY 2022 Jun;150:112978. (PubMed: 35462332) [IF=7.5]

8). Yu L et al. Formononetin protects against inflammation associated with cerebral ischemia-reperfusion injury in rats by targeting the JAK2/STAT3 signaling pathway. BIOMEDICINE & PHARMACOTHERAPY 2022 May;149:112836. (PubMed: 35339827) [IF=7.5]

9). Zhao Y et al. Demethyleneberberine alleviated the inflammatory response by targeting MD-2 to inhibit the TLR4 signaling. Frontiers in Immunology 2023;14(1130404) (PubMed: 37168866) [IF=7.3]

Application: WB    Species: Mouse    Sample: colonic tissue

Figure 3 DMB inhibited TLR4 signaling in a MyD88-dependent and -independent manner. (A) The protein expressions were assessed by immunoblotting for IL-1β, IκB, and p-IκB (Ser32) in colonic tissue; GAPDH served as reference. (B) The grayscale analysis of IL-1β and the ratio of p-IκB/IκB. (C) The protein expression of MyD88, TRAF6, and IRF3 in colonic tissue; GAPDH served as reference. (D) The grayscale analysis of MyD88, TTRAF6, and IRF3. (E–G) The mRNA levels of IL-1β, TNF-α, and IFN-α in colonic tissues. Statistical analysis was performed using one-way ANOVA. n = 3. #p < 0.05, ##p < 0.01, ###p < 0.005 (#: TNBS group versus the CON group) and *p < 0.05, **p < 0.01, ***p < 0.005, ns, non-significantly (*: the DMB or BBR group versus the TNBS group).

10). Shan et al. Pediococcus pentosaceus Enhances Host Resistance Against Pathogen by Increasing IL-1β Production: Understanding Probiotic Effectiveness and Administration Duration. Frontiers in Immunology 2021 Nov 26;12:766401. (PubMed: 34899717) [IF=7.3]



产品的规格、报价、验证数据请以官网为准,官网链接:www.affbiotech.com | www.affbiotech.cn(简体中文)| www.affbiotech.jp(日本語)






Affinity Biosciences将不会对在使用我们的产品时可能发生的专利侵权或其他侵权行为负责。Affinity Biosciences, Affinity Biosciences标志和所有其他商标所有权归Affinity Biosciences LTD.