Please use this identifier to cite or link to this item: http://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
RMID: 0030022846
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
Appears in Collections:Medicine publications

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