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|Title:||ER stress does not cause upregulation and activation of caspase-2 to initiate apoptosis|
|Citation:||Cell Death and Differentiation, 2014; 21(3):475-480|
|Publisher:||Nature Publishing Group|
|JJ Sandow, L Dorstyn, LA O, Reilly, M Tailler, S Kumar, A Strasser, and PG Ekert|
|Abstract:||A recent report claimed that endoplasmic reticulum (ER) stress activates the ER trans-membrane receptor IRE1α, 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.|
|Keywords:||Caspase-2; ER stress; apoptosis|
|Rights:||© 2014 Macmillan Publishers Limited All rights reserved|
|Appears in Collections:||Medicine publications|
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