CASP8 | Caspase-8 Recombinant Rabbit mAb (一抗) - WB | Bioss

bsm-52690R

重组兔单抗

CASP8 | Caspase-8 Recombinant Rabbit mAb

半胱氨酸蛋白酶8重组兔单抗

ALPS2B; CAP4; Casp-8; FLICE; MACH; MCH5; CD20; CK-20; CK20; K20; KRT21; CASP8_HUMAN; CASP8; Apoptotic cysteine protease; Apoptotic protease Mch-5; FADD-homologous ICE/ced-3-like protease; FADD-like ICE (FLICE); ICE-like apoptotic protease 5; MORT1-associated ced-3 homolog (MACH); 3.4.22.61; CASP8_MOUSE; CASP8_RAT; caspase 8; caspase 8, apoptosis-related cysteine protease; caspase 8, apoptosis-related cysteine peptidase

Rabbit

A synthesized peptide derived from human Caspase 8: 385-435/479

IgG

Liquid

affinity purified by Protein A

Recombinant

1A14

55 kDa

57 kDa

1mg/ml

0.01M TBS (pH7.4) with 1% BSA, 0.02% Proclin300 and 50% Glycerol.

Shipped at 4℃. Store at -20℃ for one year. Avoid repeated freeze/thaw cycles.

This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.

半胱氨酸蛋白酶-8，在凋亡执行阶段起中心作用。

Caspases are cysteine proteases, expressed as inactive precursors, that mediate apoptosis by proteolysis of specific substrates. Caspases have the ability to cleave after aspartic acid residues. There are two classes of caspases involved in apoptosis; initiators (activation by receptor cluster) and effectors (activation by mitochondrial permeability transition). Proapoptotic signals autocatalytically activate initiator caspases, such as Caspase 8 and Caspase 9. Activated initiator caspases then process effector caspases, such as Caspase 3 and Caspase 7, which in turn cause cell collapse.

CASP8

Caspase-8

Heterotetramer that consists of two anti-parallel arranged heterodimers, each one formed by a 18 kDa (p18) and a 10 kDa (p10) subunit. Interacts with FADD, CFLAR and PEA15. Isoform 9 interacts at the endoplasmic reticulum with a complex containing BCAP31, BAP29, BCL2 and/or BCL2L1. Interacts with TNFAIP8L2.

Cytoplasm.

Isoform 1, isoform 5 and isoform 7 are expressed in a wide variety of tissues. Highest expression in peripheral blood leukocytes, spleen, thymus and liver. Barely detectable in brain, testis and skeletal muscle.

Defects in CASP8 are the cause of caspase-8 deficiency (CASP8D) [MIM:607271]. CASP8D is a disorder resembling autoimmune lymphoproliferative syndrome (ALPS). It is characterized by lymphadenopathy, splenomegaly, and defective CD95-induced apoptosis of peripheral blood lymphocytes (PBLs). It leads to defects in activation of T-lymphocytes, B-lymphocytes, and natural killer cells leading to immunodeficiency characterized by recurrent sinopulmonary and herpes simplex virus infections and poor responses to immunization.

Belongs to the peptidase C14A family.
Contains 2 DED (death effector) domains.

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 CASP10. 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. Isoform 5, isoform 6, isoform 7 and isoform 8 lack the catalytic site and may interfere with the pro-apoptotic activity of the complex.