Caspase-8 Antibody (YA4272)
(Synonyms: CAP4; MACH; MCH5; FLICE; ALPS2B; Casp-8; FLJ17672; MGC78473)Caspase-8 Antibody (YA4272) is a Mouse-derived and non-conjugated IgG1 monoclonal antibody, targeting to Caspase-8.
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Host:
Mouse
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Isotype:
IgG
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Application:
WB, IHC-P, FC, ELISA
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Reactivity :
Human, Mouse, Monkey, Rat
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Formulation:
Supplied in ascitic fluid containing 0.03% sodium azide.
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Conjugation:
Non-conjugated
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
Applications
| Application |
WB
WB: Western Blot
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IHC-P
IHC-P: Immunohistochemistry-Paraffin
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FC
FC: Flow Cytometry
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ELISA
ELISA: Enzyme Linked Immunosorbent Assay
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|---|---|---|---|---|
| Dilution Ratio | 1:500-1:2000 | 1:200-1:1000 | 1:200-1:400 | 1:10000 |
Product Details
Caspase-8 Antibody (YA4272) is a Mouse-derived and non-conjugated IgG1 monoclonal antibody, targeting to Caspase-8.
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Host Mouse
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Clonality Monoclonal
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Species ReactivityHuman, Mouse, Monkey, Rat
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Observed Molecular WeightObserved band size: 55 kDa
Note: Due to possible protein modifications or aggregation, the molecular weight should be confirmed by actual measurement, and the predicted value is for reference only.
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Calculated Molecular Weight Predicted band size: 55 kDa
Purified recombinant fragment of human CASP8 aa 302-464.
affinity purified.
Non-conjugated
Unmodified
IgG
Product Properties
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Appearance
Solution
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Formulation
Supplied in ascitic fluid containing 0.03% sodium azide.
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Storage & Stability
Stored at -20°C for 1 year. Avoid repeated freeze / thaw cycles.
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Shipping
Shipping with blue ice.
Background
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Function
Caspase 8 is an initiator protease of death receptor-mediated extrinsic apoptosis and also supports cell survival by restraining RIP-family kinase-dependent necroptosis[1]. Mechanistically, caspase 8 works with cFLIP to regulate the switch among survival, apoptosis, and necroptosis, while cFLIP is structurally related to caspase 8 but lacks proteolytic activity[1][2]. Therefore, caspase 8 differs from inflammatory caspases such as caspase 1, 4, 5, and 12, which participate in inflammasome-related innate immune responses[3]. In intestinal disease, caspase 8 controls Paneth cell necroptosis and may contribute to epithelial cell death and mucosal inflammation in Crohn’s disease[3]. In severe SARS-CoV-2 mouse models, non-apoptotic caspase 8 promoted cytokine release, IL-1β elevation, NF-κB-linked inflammation, and disease pathology[4]. In ovarian cancer, low caspase 8 expression correlated with shorter overall survival, while caspase 8 loss enhanced non-apoptotic necroptotic death under NF-κB blockade[5]. For experimental applications, studies use genetic caspase 8 loss, viral caspase 8 inhibitors, and necroptosis pathway modulation to separate apoptosis, inflammation, and RIPK3-MLKL-dependent cell death[6].
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Subcellular Localization
Cytoplasm; Nucleus; Cell projection, lamellipodium
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Expression
Tissue_specificity:Isomers 1, 5, and 7 are expressed in a variety of tissues. They are most highly expressed in peripheral blood leukocytes, spleen, thymus, and liver. They are almost undetectable in the brain, testes, and skeletal muscle. -
Isoforms & Post-Translational Modification
Q14790 has 9 isomers: Q14790-1: 55391 Da (predicted); Q14790-2: 53768 Da (predicted); Q14790-3: 45929 Da (predicted); Q14790-4: 57701 Da (predicted); Q14790-5: 27484 Da (predicted); Q14790-6: 25862 Da (predicted); Q14790-7: 32330 Da (predicted); Q14790-8: 30707 Da (predicted); Q14790-9: 61836 Da (predicted).
Generation of the p10 and p18 subunits requires association with the death-inducing signaling complex (DISC), whereas additional processing is likely due to the autocatalytic activity of the activated protease. GZMB and CASP10 can be involved in these processing events;Phosphorylation on Ser-387 during mitosis by CDK1 inhibits activation by proteolysis and prevents apoptosis (PubMed:20937773). Phosphorylation on Tyr-380 by SRC is mediated by interaction with the SRC SH2 domain and does not affect dimerization or recruitment to the death-inducing signaling complex (DISC) but negatively regulates DISC-mediated processing and activation of CASP8, down-regulating its proapoptotic function (PubMed:16619028, PubMed:27109099). Phosphorylation on Tyr-380 also enhances localization to lamellipodia in migrating cells (PubMed:18216014);(Microbial infection) ADP-riboxanation by C.violaceum CopC blocks CASP8 processing, preventing CASP8 activation and ability to mediate extrinsic apoptosis;(Microbial infection) Proteolytically cleaved by the cowpox virus CRMA death inhibitory protein -
Subunit
Heterotetramer that consists of two anti-parallel arranged heterodimers, each one formed by a 18 kDa (p18) and a 10 kDa (p10) subunit (PubMed:10508784). Component of the death-induced signaling complex (DISC) composed of cell surface receptor FAS/CD95 or TNFRSF1A, adapter protein FADD and the CASP8 protease; recruitment of CASP8 to the complex is required for processing of CASP8 into the p18 and p10 subunits (PubMed:8681376, PubMed:8681377, PubMed:9184224). Component of the AIM2 PANoptosome complex, a multiprotein complex that drives inflammatory cell death (PANoptosis) (By similarity). Interacts with CFLAR and PEA15 (PubMed:10442631). Interacts with TNFAIP8L2 (By similarity). Interacts with CASP8AP2 (PubMed:16378960). Interacts with RFFL and RNF34; negatively regulate CASP8 through proteasomal degradation (PubMed:15069192). Interacts with NOL3; decreases CASP8 activity in a mitochondria localization- and phosphorylation-dependent manner and this interaction is dissociated by calcium (PubMed:15509781). Interacts with UBR2ca (PubMed:28602583). Interacts with RIPK1 (By similarity). Interacts with stimulated TNFRSF10B; this interaction is followed by CASP8 proteolytic cleavage and activation (PubMed:18846110). Interacts (phosphorylated on Tyr-380) with PIK3R1 (PubMed:27109099)
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SwissProt ID
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Synonyms
CAP4; MACH; MCH5; FLICE; ALPS2B; Casp-8; FLJ17672; MGC78473
Documentation
[1]. Salvesen GS, et al. Functions of caspase 8: the identified and the mysterious. Semin Immunol. 2014 Jun;26(3):246-52. [Content Brief]
[2]. Tsuchiya Y, et al. FLIP the Switch: Regulation of Apoptosis and Necroptosis by cFLIP. Int J Mol Sci. 2015 Dec 18;16(12):30321-41. [Content Brief]
[3]. Becker C, et al. Complex roles of caspases in the pathogenesis of inflammatory bowel disease. Gastroenterology. 2013 Feb;144(2):283-293. [Content Brief]
[4]. M Bader S, et al. Non-apoptotic caspase-8 is critical for orchestrating exaggerated inflammation during severe SARS-CoV-2 infection. Nat Commun. 2025 Nov 13;16(1):9822. [Content Brief]
[5]. Kim M, et al. Caspase 8 expression may determine the survival of women with ovarian cancer. Cell Death Dis. 2016 Jan 14;7(1):e2045. [Content Brief]
[6]. Daley-Bauer LP, et al. Mouse cytomegalovirus M36 and M45 death suppressors cooperate to prevent inflammation resulting from antiviral programmed cell death pathways. Proc Natl Acad Sci U S A. 2017 Mar 28;114(13):E2786-E2795. [Content Brief]
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