|Tested species reactivity||Human, Mouse, Rat|
|Host / Isotype||Rabbit / IgG|
|Immunogen||Synthetic peptides corresponding to residues 345-359 and 366-383 of rat Caspase-9-CTD.|
|Storage buffer||PBS with 0.05% BSA|
|Contains||0.05% sodium azide|
|Storage Conditions||-20° C, Avoid Freeze/Thaw Cycles|
|Tested Applications||Dilution *|
|Western Blot (WB)||1:250-1:1000|
* Suggested working dilutions are given as a guide only. It is recommended that the user titrate the product for use in their own experiment using appropriate negative and positive controls.
Suggested positive control: Hela whole cell lysate, mouse heart protein, mouse or rat heart, or HeLa, rat heart protein.
Caspase-9 and Apaf-1 bind to each other, which leads to Caspase-9 activation. Activated caspase-9 cleaves and activates Caspase-3 that is one of the key proteases, being responsible for the proteolytic cleavage of many key proteins in apoptosis. Caspase-9 play a central role in cell death induced by a wide variety of apoptosis inducers including TNFa, TRAIL, anti-CD-95, FADD, and TRADD. Caspase-9 is expressed in variety of human tissues. Recently, a novel isoform of rat Caspase-9 has been identified in which the C terminus of full-length Caspase-9 is replaced with an alternative peptide sequence. This protein called, Casp-9-CTD (where CTD is carboxyl-terminal divergent) is expressed in multiple tissues, with the relative highest statement observed in ovary and heart. The variant C terminus of Casp-9-CTD in rat is derived from an alternative exon of the rat Caspase-9 gene. Casp-9-CTD was found primarily in the cytoplasm and was not detected in the nucleus. Caspase-9-CTD proenzyme is not processed in the cells and lacks apoptotic activity. The Casp-9-CTD transfected cells are resistant to caspases induction by cytochrome c, suggesting that Casp-9-CTD acts as a dominant-negative variant.
For Research Use Only. Not for use in diagnostic procedures. Not for resale without express authorization.