期刊
JOURNAL OF CELL BIOLOGY
卷 150, 期 4, 页码 887-894出版社
ROCKEFELLER UNIV PRESS
DOI: 10.1083/jcb.150.4.887
关键词
calcium; Alzheimer's disease; Bcl-xL; endoplasmic reticulum; ER stress
类别
Calpains and caspases are two cysteine protease families that play important roles in regulating pathological cell death. Here, we report that m-calpain may be responsible for cleaving procaspase-12, a caspase localized in the ER, to generate active caspase-12. In addition, calpain may be responsible for cleaving the loop region in Bcl-xL and, therefore, turning an antiapoptotic molecule into a proapoptotic molecule. We propose that disturbance to intracellular calcium storage as a result of ischemic injury or amyloid beta peptide cytotoxicity may induce apoptosis through calpain-mediated caspase-12 activation and Bcl-xL inactivation. These data suggest a novel apoptotic pathway involving calcium-mediated calpain activation and cross-talks between calpain and caspase families.
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