Caspase, Cleaved BioAssay(TM) Sample Kit

Check status of cleaved caspase, including cleaved caspase-3 (Asp175), caspase-6 (Asp162), caspase-7 (Asp198), caspase-8 (Asp384) monoclonal, caspase-9 (Asp315) and (Asp330) (human specific). The kit contains enough primary and secondary antibodies to perform four Western mini-blot experiments with each primary antibody.\n\nApoptosis, or programmed cell death, 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, a-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-a, 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 calciummediated activation of caspase-12. The inhibitor of apoptosis protein (IAP) family includes XIAP and Survivin and functions by binding and inhibiting several caspases (4,5). 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 (6). The Cleaved Caspase Antibody Sampler Kit provides an economical means to evaluate the acti-Products Included Product.

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SPECIFICATIONS

Catalog Number

C2087-06

Size

6x40ul

Form

Supplied as a liquid in 10mM sodium HEPES, pH 7.5, 150mM sodium chloride, BSA, 50% glycerol.

Purity

Purified by protein A and peptide affinity chromatography.

References

(1) Baker, S.J. and Reddy, E.P. (1998) Oncogene 17, 3261-3270. (2) Budihardjo, I. et al. (1999) Annu. Rev. Cell Dev. Biol. 15, 269-290. (3) Nakagawa, T. et al. (1999) Nature 403, 98-103. (4) Deveraux, Q.L. et al. (1998) EMBO J. 17, 2215- 2223. (5) Li, F. et al. (1998) Nature 396, 580-584. (6) Du, C. et al. (2000) Cell 102, 33-42.