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First published online September 20, 2006

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Mitochondrial executioner for the terminally (ER) stressed

The accumulation of misfolded proteins in cells induces ER stress, which can lead to apoptosis. But what is the molecular mechanism that links these processes? On p. 3958, Hiroki Yoshida and co-authors report that ER-stress-induced apoptosis depends on the mitochondrial apoptosis pathway and involves Apaf1 - a component of the `apoptosome' that activates caspases in this pathway. They show that Apaf-1-deficient mouse embryonic fibroblasts (MEFs) are more resistant than wild-type cells to tunicamycin, which induces ER stress. In addition, they demonstrate that ER stress does not activate the downstream executioner caspase-3 in Apaf-1-deficient MEFs. Significantly, the authors show that Apaf-1 is involved in ER-stress-induced apoptosis in vivo - tunicamycin-induced apoptosis in the kidneys of Apaf-1-deficient mice is reduced compared with wild-type mice They also use overexpression studies and RNAi to dispel the earlier notion that caspase-12 - a caspase involved in inflammation - has a major role in ER-stress-induced apoptosis. Given that this process plays a role in various neurodegenerative conditions, these findings have important implications for potential treatments for these diseases.

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Related articles in JCS:

ER stress-induced apoptosis and caspase-12 activation occurs downstream of mitochondrial apoptosis involving Apaf-1

Hiroshi Shiraishi, Hideaki Okamoto, Akihiko Yoshimura, and Hiroki Yoshida
JCS 2006 119: 3958-3966. [Abstract] [Full Text]  

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Related articles in JCS Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Search for Related Content Social Bookmarking                         What's this?