|Application ||WB, IHC, IF|
|Reactivity||Human, Mouse, Rat|
|Calculated MW||49736 Da|
|Other Names||Caspase-5, CASP-5, ICE(rel)-III, Protease ICH-3, Protease TY, Caspase-5 subunit p20, Caspase-5 subunit p10, CASP5, ICH3|
|Target/Specificity||A synthetic peptide corresponding to N-terminal residues of human Caspase-5 was used as an immunogen. Based on amino acids homology, this antibody will not recognize either p20 or p10 subunits of Caspase-5.|
|Format||50 mM Tris-Glycine (pH 7.4), 0.15 M NaCl, 40% Glycerol, 0.01% sodium azide and 0.05% BSA.|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.|
|Precautions||Caspase-5 Antibody is for research use only and not for use in diagnostic or therapeutic procedures.|
|Function||Mediator of programmed cell death (apoptosis).|
|Tissue Location||Expressed in barely detectable amounts in most tissues except brain, highest levels being found in lung, liver and skeletal muscle|
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Provided below are standard protocols that you may find useful for product applications.
Caspases are a family of cytosolic aspartate-specific cysteine proteases involved in the initiation and execution of apoptosis. Caspase-5 (ICH-3, ICEREL-III, TY protease) is a member of the caspase-1 subfamily and it is an upstream mediator of apoptosis. Caspase-5 is highly expressed in lung, liver, and skeletal muscle, and similar to Caspase-4, its overexpression can induce cellular apoptosis (1). A tetramer, Caspase-5 separates into two subunits of a 20kda (p20) and 10kda (p10) after activation. In vitro, Caspase-5 can be cleaved by GranB, a major player in Cytotoxic T lymphocytes (CTL) induced apoptosis (2). In vivo, the Caspase-5 expression is elevated by LPS and IFNg. Caspase-5 induced apoptosis can be inhibited by CrmA and Bcl-2. Caspase-5 has also been implicated in cellular inflammatory response and in the microsatellite mutator pathway for cancer (3).
1. Kamada S, et al. Cell Death Differ 4:473-478. 1997.
2. Wang S. et al. J. Biol. Chem. 271: 20580-20587, 1996.
3. Schwartz S, et al. Cancer Res 59:2995-3002, 1999.
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