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https://hdl.handle.net/2440/100172
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Type: | Journal article |
Title: | ER stress does not cause upregulation and activation of caspase-2 to initiate apoptosis |
Author: | Sandow, J. Dorstyn, L. O'Reilly, L. Tailler, M. Kumar, S. Strasser, A. Ekert, P. |
Citation: | Cell Death and Differentiation, 2014; 21(3):475-480 |
Publisher: | Nature Publishing Group |
Issue Date: | 2014 |
ISSN: | 1350-9047 1476-5403 |
Statement of Responsibility: | 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 |
DOI: | 10.1038/cdd.2013.168 |
Grant ID: | http://purl.org/au-research/grants/nhmrc/1022916 http://purl.org/au-research/grants/nhmrc/1021456 http://purl.org/au-research/grants/nhmrc/1043057 http://purl.org/au-research/grants/nhmrc/1009145 http://purl.org/au-research/grants/nhmrc/1016701 |
Published version: | http://dx.doi.org/10.1038/cdd.2013.168 |
Appears in Collections: | Aurora harvest 3 Medicine publications |
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