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Rabbit Anti-Caspase 8 Polyclonal Antibody
Purified Rabbit Polyclonal Antibody (Pab)
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application 
| WB, IF, IHC-P |
|---|---|
| Primary Accession | O89110 |
| Reactivity | Human, Mouse, Rat |
| Host | Rabbit |
| Clonality | Polyclonal |
| Calculated MW | 55357 Da |
| Gene ID | 12370 |
|---|---|
| Other Names | MACH; Mch5; FLICE; CASP-8; Caspase-8; Casp8 |
| Dilution | WB~~1:100~1:500 |
| Format | 0.01M TBS(pH7.4), 0.09% (W/V) sodium azide and 50% Glyce |
| Storage | Store at -20 ℃ for one year. Avoid repeated freeze/thaw cycles. When reconstituted in sterile pH 7.4 0.01M PBS or diluent of antibody the antibody is stable for at least two weeks at 2-4 ℃. |
| Name | CASP8 |
|---|---|
| Function | Thiol protease that plays a key role in programmed cell death by acting as a molecular switch for apoptosis, necroptosis and pyroptosis, and is required to prevent tissue damage during embryonic development and adulthood (PubMed:12065591, PubMed:18455983, PubMed:30361383, PubMed:30381458, PubMed:31511692, PubMed:31748744, PubMed:33397971). Initiator protease that induces extrinsic apoptosis by mediating cleavage and activation of effector caspases responsible for FAS/CD95-mediated and TNFRSF1A-induced cell death (PubMed:9654089, PubMed:9837723, PubMed:24813849, PubMed:24813850). Cleaves and activates effector caspases CASP3, CASP4, CASP6, CASP7, CASP9 and CASP10 (By similarity). Binding to the adapter molecule FADD recruits it to either receptor FAS/CD95 or TNFRSF1A (PubMed:29440439). The resulting aggregate called the death-inducing signaling complex (DISC) performs CASP8 proteolytic activation (By similarity). The active dimeric enzyme is then liberated from the DISC and free to activate downstream apoptotic proteases (By similarity). Proteolytic fragments of the N-terminal propeptide (termed CAP3, CAP5 and CAP6) are likely retained in the DISC (By similarity). In addition to extrinsic apoptosis, also acts as a negative regulator of necroptosis: acts by cleaving RIPK1 at 'Asp-325', which is crucial to inhibit RIPK1 kinase activity, limiting TNF-induced apoptosis, necroptosis and inflammatory response (PubMed:31511692). Also able to initiate pyroptosis by mediating cleavage and activation of gasdermin-C and -D (GSDMC and GSDMD, respectively): gasdermin cleavage promotes release of the N- terminal moiety that binds to membranes and forms pores, triggering pyroptosis (PubMed:30361383, PubMed:30381458). Initiates pyroptosis following inactivation of MAP3K7/TAK1 (PubMed:30361383, PubMed:30381458). Also acts as a regulator of innate immunity by mediating cleavage and inactivation of N4BP1 downstream of TLR3 or TLR4, thereby promoting cytokine production (PubMed:32971525). May participate in the Granzyme B (GZMB) cell death pathways (By similarity). Cleaves PARP1 and PARP2 (PubMed:12065591). |
| Cellular Location | Cytoplasm. Nucleus. Note=Translocates into the nucleus during apoptosis. |
| Tissue Location | Expressed in a wide variety of tissues. Highest expression in spleen, thymus, lung, liver and kidney. Lower expression in heart, brain, testis and skeletal muscle |
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Provided below are standard protocols that you may find useful for product applications.
Background
Most upstream protease of the activation cascade of caspases responsible for the TNFRSF6/FAS mediated and TNFRSF1A induced cell death. Binding to the adapter molecule FADD recruits it to either receptor. The resulting aggregate called death-inducing signaling complex (DISC) performs CASP8 proteolytic activation. The active dimeric enzyme is then liberated from the DISC and free to activate downstream apoptotic proteases. Proteolytic fragments of the N-terminal propeptide (termed CAP3, CAP5 and CAP6) are likely retained in the DISC. Cleaves and activates CASP3, CASP4, CASP6, CASP7, CASP9 and CASP1. May participate in the GZMB apoptotic pathways. Cleaves ADPRT. Hydrolyzes the small-molecule substrate, Ac-Asp-Glu-Val-Asp-|-AMC. Likely target for the cowpox virus CRMA death inhibitory protein.
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