IL1B Antibody (Center) (Ascites)
Mouse Monoclonal Antibody (Mab)
- SPECIFICATION
- CITATIONS: 1
- PROTOCOLS
- BACKGROUND
Application
| WB, E |
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Primary Accession | P01584 |
Other Accession | P14628, P79182, NP_000567.1 |
Reactivity | Human |
Predicted | Monkey, Rabbit |
Host | Mouse |
Clonality | Monoclonal |
Isotype | IgG1 |
Clone/Animal Names | 614CT4.3.1 |
Calculated MW | 30748 Da |
Antigen Region | 148-174 aa |
Gene ID | 3553 |
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Other Names | Interleukin-1 beta, IL-1 beta, Catabolin, IL1B, IL1F2 |
Target/Specificity | This IL1B antibody is generated from mice immunized with a KLH conjugated synthetic peptide between 148-174 amino acids from the Central region of human IL1B. |
Dilution | WB~~1:2000~4000 |
Format | Mouse monoclonal antibody supplied in crude ascites with 0.09% (W/V) sodium azide. |
Storage | Maintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles. |
Precautions | IL1B Antibody (Center) (Ascites) is for research use only and not for use in diagnostic or therapeutic procedures. |
Name | IL1B (HGNC:5992) |
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Synonyms | IL1F2 |
Function | Potent pro-inflammatory cytokine (PubMed:10653850, PubMed:12794819, PubMed:28331908, PubMed:3920526). 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 (PubMed:3920526). Promotes Th17 differentiation of T-cells. Synergizes with IL12/interleukin-12 to induce IFNG synthesis from T-helper 1 (Th1) cells (PubMed:10653850). Plays a role in angiogenesis by inducing VEGF production synergistically with TNF and IL6 (PubMed:12794819). Involved in transduction of inflammation downstream of pyroptosis: its mature form is specifically released in the extracellular milieu by passing through the gasdermin-D (GSDMD) pore (PubMed:33377178, PubMed:33883744). Acts as a sensor of S.pyogenes infection in skin: cleaved and activated by pyogenes SpeB protease, leading to an inflammatory response that prevents bacterial growth during invasive skin infection (PubMed:28331908). |
Cellular Location | Cytoplasm, cytosol. Secreted. Lysosome Secreted, extracellular exosome {ECO:0000250|UniProtKB:P10749} Note=The precursor is cytosolic (PubMed:15192144). In response to inflammasome-activating signals, such as ATP for NLRP3 inflammasome or bacterial flagellin for NLRC4 inflammasome, cleaved and secreted (PubMed:24201029, PubMed:33377178, PubMed:33883744). Mature form is secreted and released in the extracellular milieu by passing through the gasdermin-D (GSDMD) pore (PubMed:33883744). In contrast, the precursor form is not released, due to the presence of an acidic region that is proteolytically removed by CASP1 during maturation (PubMed:33883744). The secretion is dependent on protein unfolding and facilitated by the cargo receptor TMED10 (PubMed:32272059) |
Tissue Location | Expressed in activated monocytes/macrophages (at protein level). |
Provided below are standard protocols that you may find useful for product applications.
Background
The protein encoded by this gene is a member of the interleukin 1 cytokine family. This cytokine is produced by activated macrophages as a proprotein, which is proteolytically processed to its active form by caspase 1 (CASP1/ICE). This cytokine is an important mediator of the inflammatory response, and is involved in a variety of cellular activities, including cell proliferation, differentiation, and apoptosis. The induction of cyclooxygenase-2 (PTGS2/COX2) by this cytokine in the central nervous system (CNS) is found to contribute to inflammatory pain hypersensitivity. This gene and eight other interleukin 1 family genes form a cytokine gene cluster on chromosome 2. [provided by RefSeq].
References
Lee, B., et al. J. Immunol. 185(10):5926-5934(2010)
Arana-Argaez, V.E., et al. J. Biol. Chem. 285(43):32824-32833(2010)
Zhang, Z., et al. J. Biol. Chem. 285(43):33092-33103(2010)
Wang, D., et al. Nat. Immunol. 11(10):905-911(2010)
Gein, O.N., et al. Patol Fiziol Eksp Ter 1, 10-13 (2010) :
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