Apoptosis Antibody Kit

Apoptosis (Caspase & Bcl-2 family) Antibody sampler kits

Cat. Num. AAA2550156

• Applications: Western Blot
• Synonyms: Apoptosis; Apoptosis (Caspase & Bcl-2 family) Antibody sampler kits; Apoptosis antibody kit

• Applicable Applications for Apoptosis antibody kit: Western Blot (WB)

Western Blot (WB)

(Western Blot analysis of various cells using Cleaved-Caspase-3 p17 (D175) Polyclonal Antibody at dilution of 1:1000.)

Western Blot (WB)

(Western Blot analysis of Mouse spleen using Cleaved-Caspase-8 p18 (S217) Polyclonal Antibody at dilution of 1:1000.)

Western Blot (WB)

(Western Blot analysis of VEC, A549 cells using Cleaved-Caspase-9 p35 (D315) Polyclonal Antibody at dilution of 1:1000.)

Western Blot (WB)

(Western Blot analysis of COS-7 cells using Bcl-2 Polyclonal Antibody at dilution of 1:1000.)

Western Blot (WB)

(Western Blot analysis of HepG2 cells using Bax Polyclonal Antibody at dilution of 1:1000.)

Western Blot (WB)

(Western Blot analysis of Rat musle cells using BID Polyclonal Antibody at dilution of 1:1000.)

Related Product Information for Apoptosis antibody kit

Background: Apoptosis is a regulated physiological process leading to cell death. Caspases, a family of cysteine acid proteases, are central regulators of apoptosis. Initiator caspases (including 8, 9, 10 and 12) are closely coupled to proapoptotic signals. Once activated, these caspases cleave and activate downstream effector caspases (including 3, 6 and 7), which in turn cleave cytoskeletal and nuclear proteins like PARP, alpha-fodrin, DFF and lamin A, and induce apoptosis. Cytochrome c released from mitochondria is coupled to the activation of caspase-9, a key initiator caspase. Proapoptotic stimuli include the FasL, TNF-alpha, DNA damage and ER stress. Fas and TNFR activate caspases 8 and 10, DNA damage leads to the activation of caspase-9 and ER stress leads to the calcium-mediated activation of caspase-12. The inhibitor of apoptosis protein (IAP) family includes XIAP and survivin and functions by binding and inhibiting several caspases. Smac/Diablo, a mitochondrial protein, is released into the cytosol upon mitochondrial stress and competes with caspases for binding of IAPs. The interaction of Smac/Diablo with IAPs relieves the inhibitory effects of the IAPs on caspases.The Bcl-2 family consists of a number of evolutionarily conserved proteins containing Bcl-2 homology domains (BH) that regulate apoptosis through control of mitochondrial membrane permeability and release of cytochrome c (1-3). Four BH domains have been identified (BH1-4) that mediate protein interactions. The family can be separated into three groups based upon function and sequence homology: pro-survival members include Bcl-2, Bcl-xL, Mcl-1, A1 and Bcl-w; pro-apoptotic proteins include Bax, Bak and Bok, and "BH3 only" proteins Bad, Bik, Bid, Puma, Bim, Bmf, Noxa and Hrk. Interactions between death-promoting and death-suppressing Bcl-2 family members has led to a rheostat model in which the ratio of pro-apoptotic and anti-apoptotic proteins controls cell fate (4). Thus, pro-survival members exert their behavior by binding to and antagonizing death- promoting members. In general, the "BH3-only members" can bind to and antagonize the pro-survival proteins leading to increased apoptosis (5). While some redundancy of this system likely exists, tissue specificity, transcriptional and post-translational regulation of many of these family members can account for distinct physiological roles.