The endoplasmic reticulum stress sensor IRE1α protects cells from apoptosis induced by the coronavirus infectious bronchitis virus.

ABSTRACT:

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The unfolded-protein response (UPR) is a signal transduction cascade triggered by perturbation of the homeostasis of the endoplasmic reticulum (ER). UPR resolves ER stress by activating a cascade of cellular responses, including the induction of molecular chaperones, translational attenuation, ER-associated degradation, and other mechanisms. Under prolonged and irremediable ER stress, however, the UPR can also trigger apoptosis. Here, we report that in cells infected with the avian coronavirus infectious bronchitis virus (IBV), ER stress was induced and the IRE1α-XBP1 pathway of UPR was activated. Knockdown and overexpression experiments demonstrated that IRE1α protects infected cells from IBV-induced apoptosis, which required both its kinase and RNase activities. Our da

SUBMITTER: Fung TS 

PROVIDER: S-EPMC4248946 | biostudies-literature | 2014 Nov

REPOSITORIES: biostudies-literature