【摘 要】
：
Ectopic expression of the N-terminal fragment resulting from the partial cleavage of RasGAP by caspases results in the activation of the anti-apoptotic Ras-
【机 构】
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InstituteofCellularBiologyandMorphology(IBCM),UniversityofLausanne,Switzerland
【出 处】
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2005 World DNA and Genome Day(2005中国(大连)国际DNA和基因组节大会)
论文部分内容阅读
Ectopic expression of the N-terminal fragment resulting from the partial cleavage of RasGAP by caspases results in the activation of the anti-apoptotic Ras-PI3K-Akt pathway.Here we demonstrate that this fragment is generated in a caspase-3-dependent manner in stressed cells that do not undergo apoptosis.Subjected to the same low stress conditions,cells,in which the wild-type RasGAP protein was replaced with an uncleavable mutant,could not activate Akt,could not prevent an amplification of the caspase-3 activity,and eventually underwent apoptosis.Formation of fragment N in response to low caspase-3 activation is therefore critical for survival of stressed cells.Executioner caspases control therefore the extent of their own activation by a feedback regulatory mechanism initiated by the partial cleavage of RasGAP.
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