Product: Cleaved-IL-1 beta (Asp116) Antibody
Catalog: AF4006
Source: Rabbit
Application: WB, IHC, IF/ICC
Reactivity: Human, Mouse, Rat, Zebrafish
Mol.Wt.: 17 kD; 31kD(Calculated).
Uniprot: P01584
RRID: AB_2801567

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Product Info

Source:
Rabbit
Application:
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.
*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,Rat,Zebrafish
Clonality:
Polyclonal
Specificity:
Cleaved-IL-1 beta (Asp116) Antibody detects endogenous levels of fragment of activated IL-1 beta resulting from cleavage adjacent to Asp116.
RRID:
AB_2801567
Cite Format: Affinity Biosciences Cat# AF4006, RRID:AB_2801567.
Purification:
The antiserum was purified by peptide affinity chromatography using SulfoLink™ Coupling Resin (Thermo Fisher Scientific).
Storage:
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.
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:
Uniprot:
Gene(ID):
Expression:
P01584 IL1B_HUMAN:

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

Sequence:
MAEVPELASEMMAYYSGNEDDLFFEADGPKQMKCSFQDLDLCPLDGGIQLRISDHHYSKGFRQAASVVVAMDKLRKMLVPCPQTFQENDLSTFFPFIFEEEPIFFDTWDNEAYVHDAPVRSLNCTLRDSQQKSLVMSGPYELKALHLQGQDMEQQVVFSMSFVQGEESNDKIPVALGLKEKNLYLSCVLKDDKPTLQLESVDPKNYPKKKMEKRFVFNKIEINNKLEFESAQFPNWYISTSQAENMPVFLGGTKGGQDITDFTMQFVSS

PTMs - P01584 As Substrate

Site PTM Type Enzyme
Y140 Phosphorylation
S200 Phosphorylation
S269 Phosphorylation

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).

Subunit Structure:

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.

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). Ou W et al. Hypoxic acclimation improves cardiac redox homeostasis and protects heart against ischemia-reperfusion injury through upregulation of O-GlcNAcylation. Redox Biol 2021 Jul;43:101994. (PubMed: 33964586) [IF=10.787]

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). Shan C et al. Pediococcus pentosaceus Enhances Host Resistance Against Pathogen by Increasing IL-1β Production: Understanding Probiotic Effectiveness and Administration Duration. Front Immunol 2021 Nov 26;12:766401. (PubMed: 34899717) [IF=8.786]

3). Xia C et al. Autophagy and Exosome Coordinately Enhance Macrophage M1 Polarization and Recruitment in Influenza A Virus Infection. Front Immunol 2022 Mar 17;13:722053. (PubMed: 35371077) [IF=8.786]

Application: WB    Species: mouse    Sample: macrophages

FIGURE s4 |The total proteins of infected primary peritoneal macrophages were extracted at 24, 36, 48, and 72 h post-infection and then subjected for Western blotting. The corresponding antibodies were used to analyze autophagic protein (LC3, p62), exosome marker (CD63), and IL-1β activation pathway (IL-1β, cleaved IL-1β, and caspase-1) normalized to GAPDH.

Application: IF/ICC    Species: mouse    Sample: lung

FIGURE 3 | M1 polarization and LC3/CD63/IL-1b analysis of infected ANA-1 macrophages. Total RNA was isolated from infected ANA-1 cells at 24-h post-infection and used for transcriptional analysis of the related genes.(J) Cleaved IL-1b cellular immunofluorescence. Scale bar: 50 mm

4). Zhang LQ et al. DKK3 ameliorates neuropathic pain via inhibiting ASK-1/JNK/p-38-mediated microglia polarization and neuroinflammation. J Neuroinflammation 2022 Jun 3;19(1):129. (PubMed: 35658977) [IF=8.322]

5). Sun Z et al. Inhibition of SGLT1 protects against glycemic variability-induced cardiac damage and pyroptosis of cardiomyocytes in diabetic mice. Life Sci 2021 Jan 25;119116. (PubMed: 33508297) [IF=6.780]

Application: WB    Species: mice    Sample: left ventricle tissues

Fig. 6. Knockdown of SGLT1 suppresses inflammatory response and pyroptosis in GVDM mice. A, Protein levels of NLRP3, ASC and caspase-1 (p20) in left ventricle tissues were measured by western blot. B, Quantitative analysis of relative protein levels of NLRP3, ASC and caspase-1. C, Protein levels of full length GSDMD and cleaved GSDMD were measured by western blot. D, Quantitative analysis of relative protein levels of cleaved GSDMD. E, The expression of NLRP3 was detected by immunofluorescence. Scale bar: 50 μm. F, Caspase-1 activity was measured by commercial kit. The relative mRNA levels of IL-1β (G) and IL-18 (H) were detected by qRT-PCR. I, The protein levels of IL-1β, pro-IL-1β and IL-18 were measured by western blot. Quantitative analysis of relative protein levels of IL-1β (J) and IL-18 (K). The release of IL-1β (L) and IL-18 (M) were detected by ELISA. Data were expressed as mean ± Standard deviation (SD). ***p < 0.001, **p < 0.01, *p < 0.05 vs control mice; †††p < 0.001, ††p < 0.01, † p < 0.05 vs DM mice; ###p < 0.001, ##p < 0.01 vs GVDM+shNC mice. DM, diabetes mellitus; GV, glycemic variability; SGLT1, sodium-glucose cotransporter 1; shSGLT1, SGLT1 shRNA; shNC, negative control shRNA; NLRP3, NLR family pyrin domain containing 3; ASC, apoptosis-associated speck-like protein containing CARD domain; GSDMD, gasdermin D.

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=6.656]

7). Yu S et al. Novel insights into antidepressant mechanism of Kai Xin San formula: Inhibiting NLRP3 inflammasome activation by promoting autophagy. Phytomedicine 2021 Dec;93:153792. (PubMed: 34735906) [IF=6.656]

8). He Q et al. Parkin-Dependent Mitophagy is Required for the Inhibition of ATF4 on NLRP3 Inflammasome Activation in Cerebral Ischemia-Reperfusion Injury in Rats. Cells 2019 Aug 14;8(8) (PubMed: 31416289) [IF=6.600]

9). Wang M et al. Icariin attenuates renal fibrosis in chronic kidney disease by inhibiting interleukin‐1β/transforming growth factor‐β‐mediated activation of renal fibroblasts. Phytother Res 2021 Nov;35(11):6204-6215. (PubMed: 34426999) [IF=6.388]

Application: WB    Species: Rat    Sample:

FIGURE 2 Icariin inhibited the secretion of pro-inflammatory cytokine IL-1β in 5/6 (A/I) rats. (A) The location between CD68 and α-SMA proteins was analyzed by IF double staining. 200 magnification (B) The protein content of NF-κB in cytosolic and nuclear fractions was detected by immunoblotting. GAPDH and Lamin B1 were used as loading controls. (C) Quantitative analysis of NF-κB protein content in cytoplasm and nucleus. (D) Representative immunoblot demonstrating the content of cleaved IL-1β protein. (E) Quantification of cleaved IL-1β level. (F) The concentration of IL-1β in circulation was detected by ELISA method. (G) The serum levels of total antioxidant capacity were measured by the ABTS method. (H) Determination of Mn-SOD activity in kidney tissues by the WST-8 method. (I) Determination of MDA content in kidney tissues by the TBA method. n = 3–6 per group. Data were analyzed by One-way ANOVA with LSD post hoc tests. Values are mean ± SD. **p < 0.01, ***p < 0.001 versus Sham, # p < 0.05, ##p < 0.01, ###p < 0.001 vs. 5/6(A/I). Sham, Sham group; Sham + ICAH, Sham + Icariin high-dose group; 5/6 (A/I), 5/6 (A/I) group; 5/6 (A/I) + ICAL, 5/6 (A/I) + Icariin low-dose group; 5/6 (A/I) + ICAH, 5/6 (A/I) + Icariin high-dose group [Colour figure can be viewed at wileyonlinelibrary.com]

10). Park JH et al. Notch1-mediated inflammation is associated with endothelial dysfunction in human brain microvascular endothelial cells upon particulate matter exposure. Arch Toxicol 2020 Nov 7. (PubMed: 33159583) [IF=6.168]

Application: WB    Species: human    Sample: endothelial cells

Fig. 2 Involvement of PM10 induced endothelial dysfunction was further investigated. a HBMECs were treated for 24  h with 5, 10 and 25 μg/mL of PM10, lysed in RIPA bufer, and the lysates were probed with antibodies against NLRP3, caspase-1, cleaved-caspase-1 and cleaved IL-1β. b

Application: WB    Species: human    Sample: endothelial cells

Fig.2 c HBMECs were treated for 24 h with 25 μg/mL of PM10 in the presence or absence of MCC950 (10 nM, 3 h). Cell lysates were probed with antibodies against NLRP3, cleaved-caspase-1 and cleaved IL-1β. β-actin was used as a loading control for lysates.

Application: WB    Species: human    Sample: endothelial cells

Fig.3 f Cell lysates were probed with antibodies against NLRP3, cleaved-caspase-1 and cleaved IL-1β.

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