ER stress does not cause upregulation and activation of caspase-2 to initiate apoptosis

作者：Sandow J J; Dorstyn L; O' Reilly L A; Tailler M; Kumar S^*; Strasser A; Ekert P G

来源：Cell Death and Differentiation, 2014, 21(3): 475-480.

DOI：10.1038/cdd.2013.168

• caspase-2
• ER stress
• apoptosis

A recent report claimed that endoplasmic reticulum (ER) stress activates the ER trans-membrane receptor IRE1 alpha, leading to increased caspase-2 levels via degradation of microRNAs, and consequently induction of apoptosis. This observation casts caspase-2 into a central role in the apoptosis triggered by ER stress. We have used multiple cell types from caspase-2-deficient mice to test this hypothesis but failed to find significant impact of loss of caspase-2 on ER-stress-induced apoptosis. Moreover, we did not observe increased expression of caspase-2 protein in response to ER stress. Our data strongly argue against a critical role for caspase-2 in ER-stress-induced apoptosis.

• 出版日期2014-3
• 单位河北医科大学