IL1 beta Antibody - #DF6251

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Product: IL1 beta Antibody
Catalog: DF6251
Description: Rabbit polyclonal antibody to IL1 beta
Application: WB IHC
Reactivity: Human, Mouse, Rat
Prediction: Horse, Rabbit
Mol.Wt.: 31kDa; 31kD(Calculated).
Uniprot: P01584
RRID: AB_2838217

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

Product Info

Source:
Rabbit
Application:
WB 1:500-1:2000, IHC 1:50-1:200
*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
Prediction:
Horse(100%), Rabbit(100%)
Clonality:
Polyclonal
Specificity:
IL1 beta Antibody detects endogenous levels of total IL1 beta.
RRID:
AB_2838217
Cite Format: Affinity Biosciences Cat# DF6251, RRID:AB_2838217.
Conjugate:
Unconjugated.
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:

P01584(IL1B_HUMAN) >>Visit HPA database.

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

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

Description:
The 20S proteasome is the major proteolytic enzyme complex involved in intracellular protein degradation. PA700, PA28, and PA200 are three major protein Interleukin-1beta (IL-1beta), one of the major caspase-1 targets, is a multifunctional cytokine that is involved in a host of immune and proinflammatory responses (1). It is produced primarily by activated monocytes and macrophages. It signals through various adaptor proteins and kinases that lead to activation of numerous downstream targets (2-6). Human IL-1beta is synthesized as a 31 kDa precursor. To gain activity, the precursor must be cleaved by caspase-1 between Asp116 and Ala117 to yield a 17 kDa mature form (7,8). Detection of the 17 kDa mature form of IL-1beta is a good indicator of caspase-1 activity.
Sequence:
MAEVPELASEMMAYYSGNEDDLFFEADGPKQMKCSFQDLDLCPLDGGIQLRISDHHYSKGFRQAASVVVAMDKLRKMLVPCPQTFQENDLSTFFPFIFEEEPIFFDTWDNEAYVHDAPVRSLNCTLRDSQQKSLVMSGPYELKALHLQGQDMEQQVVFSMSFVQGEESNDKIPVALGLKEKNLYLSCVLKDDKPTLQLESVDPKNYPKKKMEKRFVFNKIEINNKLEFESAQFPNWYISTSQAENMPVFLGGTKGGQDITDFTMQFVSS

Predictions

Predictions:

Score>80(red) has high confidence and is suggested to be used for WB detection. *The prediction model is mainly based on the alignment of immunogen sequences, the results are for reference only, not as the basis of quality assurance.

Species
Results
Score
Rabbit
100
Horse
100
Pig
75
Bovine
75
Sheep
75
Dog
0
Xenopus
0
Zebrafish
0
Chicken
0
Model Confidence:
High(score>80) Medium(80>score>50) Low(score<50) No confidence

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). Inhibition of the NLRP3-inflammasome prevents cognitive deficits in experimental autoimmune encephalomyelitis mice via the alteration of astrocyte phenotype. Cell Death & Disease (PubMed: 32415059) [IF=9.0]

Application: WB    Species: mouse    Sample: hippocampus

Fig.S1|The levels of pro-IL1β, IL-18, ASC, and cleaved caspase-1 p10 were increased,and pretreatment with MCC950 decreased the expression of these proteins (Figs. 1c and S1C).
2). Highly Acylated Anthocyanins from Purple Sweet Potato ( Ipomoea batatas L.) Alleviate Hyperuricemia and Kidney Inflammation in Hyperuricemic Mice: Possible Attenuation Effects on Allopurinol. Journal of Agricultural and Food Chemistry (PubMed: 31091873) [IF=6.1]

Application: WB    Species: mouse    Sample: renal

Figure 4.| Western blot of HAA-PSP, allopurinol, and their combination on protein expression for TNF-α, TGF-β1, IL-6, IL-1β, ICAM-1, COX-2,and NF-κB p65 in renal tissue of hyperuricemic mice. The contents of target proteins were normalized to GAPDH. Values are expressed as the means ± SD (n = 8). Different letters marked above the bars are significantly different by an ANOVA multiple test (p < 0.05).
3). Nr2e1 deficiency aggravates insulin resistance and chronic inflammation of visceral adipose tissues in a diet-induced obese mice model. LIFE SCIENCES (PubMed: 33915130) [IF=6.1]

Application: WB    Species: mice    Sample: adipose tissues

Fig. 5. Nr2e1 deficiency exacerbated inflammation in EAT. Comparison of the epididymal fat weight (A). The ratio of epididymal fat weight to the total body weight (B). The mRNA expression of F4/80 (C). The mRNA and protein expressions of IL-6, IL-1β, TNF-α and MCP-1 (E, F). The protein levels of p-IKKβ/IKKβ, p-P65/P65 (G, H). The data are expressed as means ± SEM. *P < 0.05, **P < 0.01. ns: not significant.
4). Thalidomide Alleviates Pulmonary Fibrosis Induced by Silica in Mice by Inhibiting ER Stress and the TLR4-NF-κB Pathway. International Journal of Molecular Sciences (PubMed: 35628464) [IF=5.6]

Application: WB    Species: Mice    Sample: MH-S cells

Figure 5 Silica activated the ER stress, TLR4-NF-κB pathway as well as inflammatory response in macrophages. (A–M) Expression levels of p-PERK, p-eIF-2α, p-IRE-1α, TLR4, MyD88, p-IκBα, p-NF-κB, TNF-α, IL-6, and IL-1β in MH-S cells treated with SiO2 at different doses measured by Western blot. * Compared with control group, p < 0.05. Data are presented as the mean ± SD, n = 3 per group.
5). Effect of Sex Differences in Silicotic Mice. International Journal of Molecular Sciences (PubMed: 36430681) [IF=5.6]

Application: WB    Species: Mouse    Sample: lung tissues

Figure 4 Western blot of CD68, COL I, vimentin, and α-SMA in male and female mice exposed to silica for two, four, six weeks, and the control groups. (A) Immunohistochemical staining was used to detect the expression of CD68 in the mouse lung tissues, arrow: CD68-positive cells (brown) (scale bar = 50 µm). (B–G) Expression levels of Col I, α-SMA, vimentin, IL 6 and IL 1β in the lungs of mice were measured using the western blot. Data are presented as the mean ± SD, n = 5 per group ((B,C)—2W, (D,E)—4W, (F,G)—6W).
6). Substance P Mediates Estrogen Modulation Proinflammatory Cytokines Release in Intervertebral Disc. INFLAMMATION (PubMed: 32965648) [IF=5.1]

Application: IHC    Species: mouse    Sample: NP cells

Fig. 4.| Effects of SP agonist on E2 induced changes of TNF-α, IL-1β, and IL-6 immunohistochemical staining density. TNF-α, IL-1β, and IL-6 staining densities were increased by OVX and reversed by estrogen replacement. However, the estrogen-induced decrease was significantly inhibited by SP agonist.a–d Changes in TNF-α staining density. e–h Changes in IL-1β staining density.
7). Nr2e1 ablation impairs liver glucolipid metabolism and induces inflammation, high-fat diets amplify the damage. Biomedicine & Pharmacotherapy (PubMed: 31590127) [IF=4.8]

Application: IHC    Species: mouse    Sample: liver

Fig. 5. | Nr2e1 ablation induced hepatic inflammation, the change was aggravated by HFD treatment.. Expression of IL-1β in the liver was determined by IHC staining (n = 3; magnification, × 400) (5D) and semi-quantitatively analyzed by score system (5E).
8). Thalidomide Attenuates Skin Lesions and Inflammation in Rosacea-Like Mice Induced by Long-Term Exposure of LL-37. Drug design, development and therapy (PubMed: 36483458) [IF=4.8]

Application: WB    Species: Mouse    Sample:

Figure 5 Western blot of TNF-α and IL-1β protein expression in dorsal skin. Data are presented as the mean ± SD, n=3 for each group.
9). Microtubule affinity regulating kinase 4 promoted activation of the NLRP3 inflammasome-mediated pyroptosis in periodontitis. Journal of Oral Microbiology (PubMed: 34992737) [IF=4.5]

Application: WB    Species: Mouse    Sample: BMDMs

Figure 2. Upregulated MARK4 expression and pyroptosis in the P. gingivalis-infected BMDMs (a) BMDMs induced by L929 conditional medium for 7 days or 10 days were identified by flow cytometry. Mature BMDMs were defined as CD11b+F4/80+ cultures. (b) BMDMs were infected with P. gingivalis (MOI = 10, 50 or 250) for 2 h, and gene transcription levels were assessed by real-time qPCR (n = 3). (c) Protein expression was analyzed by Western blot after bacterial infection for 24 h (MOI = 50) (n = 3). (d) IL-Iβ in the culture supernatant was detected by ELISA. *p < 0.05; **p < 0.01; ***p < 0.001 compared with the control group.
10). miR-339-3p promotes AT1-AA-induced vascular inflammation by upregulating NFATc3 protein expression in vascular smooth muscle cells: miR-339-3p aggravates vascular inflammation. Acta Biochimica et Biophysica Sinica (PubMed: 36825443) [IF=3.7]

Application: WB    Species: Rat    Sample:

Figure 3 Antagomir-339-3p can reverse AT1-AA-induced high expression of inflammatory cytokines in rat thoracic aorta and VSMCs (A) Experimental design of the inhibition of miR-339-3p by antagomir-339-3p in AT1-AA-positive rats and in VSMCs. (B) Antagomir-339-3p effectively inhibited the content of miR-339-3p in rat thoracic aorta and VSMCs. (C) The protein expression levels of the inflammatory cytokines IL-6, IL-1β and TNF-α in vascular tissue were detected by western blot analysis after inhibiting miR-339-3p in AT1-AA-positive rats. (D) After inhibiting the expression of miR-339-3p, VSMCs were treated with AT1-AA, and the protein expression levels of IL-6, IL-1β and TNF-α in the cells were detected by western blot analysis. Data are presented as the mean±standard error. n=3 or 6. * P
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