CASP4 Antibody (Center)
Purified Rabbit Polyclonal Antibody (Pab)
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application
| WB, E |
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Primary Accession | P49662 |
Reactivity | Human |
Host | Rabbit |
Clonality | polyclonal |
Isotype | Rabbit IgG |
Calculated MW | 43262 Da |
Gene ID | 837 |
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Other Names | Caspase-4, CASP-4, ICE(rel)-II, Protease ICH-2, Protease TX, Caspase-4 subunit 1, Caspase-4 subunit 2, CASP4, ICH2 |
Target/Specificity | This CASP4 antibody is generated from a rabbit immunized with a KLH conjugated synthetic peptide between 163-197 amino acids from the Central region of human CASP4. |
Dilution | WB~~1:2000 |
Format | Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is purified through a protein A column, followed by peptide affinity purification. |
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 | CASP4 Antibody (Center) is for research use only and not for use in diagnostic or therapeutic procedures. |
Name | CASP4 {ECO:0000303|PubMed:15123740, ECO:0000312|HGNC:HGNC:1505} |
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Function | Inflammatory caspase that acts as the effector of the non- canonical inflammasome by mediating lipopolysaccharide (LPS)-induced pyroptosis (PubMed:25119034, PubMed:26375003, PubMed:32109412, PubMed:34671164, PubMed:37001519, PubMed:37993712, PubMed:37993714). Also indirectly activates the NLRP3 and NLRP6 inflammasomes (PubMed:23516580, PubMed:26375003, PubMed:32109412, PubMed:7797510). Acts as a thiol protease that cleaves a tetrapeptide after an Asp residue at position P1: catalyzes cleavage of CGAS, GSDMD and IL18 (PubMed:15326478, PubMed:23516580, PubMed:26375003, PubMed:28314590, PubMed:32109412, PubMed:37993712, PubMed:37993714, PubMed:7797510). Effector of the non-canonical inflammasome independently of NLRP3 inflammasome and CASP1: the non-canonical inflammasome promotes pyroptosis through GSDMD cleavage without involving secretion of cytokine IL1B (PubMed:25119034, PubMed:25121752, PubMed:26375003, PubMed:31268602, PubMed:32109412, PubMed:37993712, PubMed:37993714). In the non-canonical inflammasome, CASP4 is activated by direct binding to the lipid A moiety of LPS without the need of an upstream sensor (PubMed:25119034, PubMed:25121752, PubMed:29520027, PubMed:32510692, PubMed:32581219, PubMed:37993712). LPS-binding promotes CASP4 activation and CASP4-mediated cleavage of GSDMD and IL18, followed by IL18 secretion through the GSDMD pore, pyroptosis of infected cells and their extrusion into the gut lumen (PubMed:25119034, PubMed:25121752, PubMed:37993712, PubMed:37993714). Also indirectly promotes secretion of mature cytokines (IL1A and HMGB1) downstream of GSDMD-mediated pyroptosis via activation of the NLRP3 and NLRP6 inflammasomes (PubMed:26375003, PubMed:32109412). Involved in NLRP3-dependent CASP1 activation and IL1B secretion in response to non-canonical activators, such as UVB radiation or cholera enterotoxin (PubMed:22246630, PubMed:23516580, PubMed:24879791, PubMed:25964352, PubMed:26173988, PubMed:26174085, PubMed:26508369). Involved in NLRP6 inflammasome- dependent activation in response to lipoteichoic acid (LTA), a cell- wall component of Gram-positive bacteria, which leads to CASP1 activation and IL1B secretion (PubMed:33377178). Involved in LPS- induced IL6 secretion; this activity may not require caspase enzymatic activity (PubMed:26508369). The non-canonical inflammasome is required for innate immunity to cytosolic, but not vacuolar, bacteria (By similarity). Plays a crucial role in the restriction of S.typhimurium replication in colonic epithelial cells during infection (PubMed:25121752, PubMed:25964352). Activation of the non-canonical inflammasome in brain endothelial cells can lead to excessive pyroptosis, leading to blood-brain barrier breakdown (By similarity). Pyroptosis limits bacterial replication, while cytokine secretion promotes the recruitment and activation of immune cells and triggers mucosal inflammation (PubMed:25121752, PubMed:25964352, PubMed:26375003). May also act as an activator of adaptive immunity in dendritic cells, following activation by oxidized phospholipid 1- palmitoyl-2-arachidonoyl- sn-glycero-3-phosphorylcholine, an oxidized phospholipid (oxPAPC) (By similarity). Involved in cell death induced by endoplasmic reticulum stress and by treatment with cytotoxic APP peptides found in Alzheimer's patient brains (PubMed:15123740, PubMed:22246630, PubMed:23661706). Cleavage of GSDMD is not strictly dependent on the consensus cleavage site but depends on an exosite interface on CASP4 that recognizes and binds the Gasdermin-D, C- terminal (GSDMD-CT) part (PubMed:32109412). Catalyzes cleavage and maturation of IL18; IL18 processing also depends of the exosite interface on CASP4 (PubMed:15326478, PubMed:37993712, PubMed:37993714). In contrast, it does not directly process IL1B (PubMed:7743998, PubMed:7797510, PubMed:7797592). During non-canonical inflammasome activation, cuts CGAS and may play a role in the regulation of antiviral innate immune activation (PubMed:28314590). |
Cellular Location | Cytoplasm, cytosol. Endoplasmic reticulum membrane; Peripheral membrane protein; Cytoplasmic side. Mitochondrion Inflammasome. Secreted Note=Predominantly localizes to the endoplasmic reticulum (ER) Association with the ER membrane requires TMEM214 (PubMed:15123740) Released in the extracellular milieu by keratinocytes following UVB irradiation (PubMed:22246630). |
Tissue Location | Widely expressed, including in keratinocytes and colonic and small intestinal epithelial cells (at protein level). Not detected in brain. |
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Provided below are standard protocols that you may find useful for product applications.
Background
Involved in the activation cascade of caspases responsible for apoptosis execution. Involved in ER-stress induced apoptosis. Cleaves caspase-1.
References
Faucheu C.,et al.EMBO J. 14:1914-1922(1995).
Munday N.A.,et al.J. Biol. Chem. 270:15870-15876(1995).
Kamens J.,et al.J. Biol. Chem. 270:15250-15256(1995).
Fernandes-Alnemri T.,et al.Submitted (JUN-1995) to the EMBL/GenBank/DDBJ databases.
Taylor T.D.,et al.Nature 440:497-500(2006).
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