Hepatic Xbp1 gene deletion promotes endoplasmic reticulum stress-induced liver injury and apoptosis

Shantel Olivares; Anne S. Henkel

doi:10.1074/jbc.M115.676239

Hepatic Xbp1 gene deletion promotes endoplasmic reticulum stress-induced liver injury and apoptosis

Shantel Olivares, Anne S. Henkel^*

^*Corresponding author for this work

Medicine, Hepatology Division

Research output: Contribution to journal › Article › peer-review

42 Scopus citations

Abstract

Background: The unfolded protein response (UPR) either restores homeostasis or promotes apoptosis in response to endoplasmic reticulum (ER) stress. Results: ER stress causes prolonged UPR activation, severe liver injury, and enhanced apoptosis in mice lacking hepatic Xbp1. Conclusion: Hepatic Xbp1 is critical for hepatic recovery from ER stress. Significance: We implicate Xbp1 in mediating the pro-survival response of the UPR.

Original language	English (US)
Pages (from-to)	30142-30151
Number of pages	10
Journal	Journal of Biological Chemistry
Volume	290
Issue number	50
DOIs	https://doi.org/10.1074/jbc.M115.676239
State	Published - Dec 11 2015

Funding

ASJC Scopus subject areas

Molecular Biology
Biochemistry
Cell Biology

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10.1074/jbc.M115.676239

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title = "Hepatic Xbp1 gene deletion promotes endoplasmic reticulum stress-induced liver injury and apoptosis",

abstract = "Background: The unfolded protein response (UPR) either restores homeostasis or promotes apoptosis in response to endoplasmic reticulum (ER) stress. Results: ER stress causes prolonged UPR activation, severe liver injury, and enhanced apoptosis in mice lacking hepatic Xbp1. Conclusion: Hepatic Xbp1 is critical for hepatic recovery from ER stress. Significance: We implicate Xbp1 in mediating the pro-survival response of the UPR.",

author = "Shantel Olivares and Henkel, {Anne S.}",

note = "Publisher Copyright: {\textcopyright} 2015 by The American Society for Biochemistry and Molecular Biology, Inc.",

year = "2015",

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AU - Henkel, Anne S.

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N2 - Background: The unfolded protein response (UPR) either restores homeostasis or promotes apoptosis in response to endoplasmic reticulum (ER) stress. Results: ER stress causes prolonged UPR activation, severe liver injury, and enhanced apoptosis in mice lacking hepatic Xbp1. Conclusion: Hepatic Xbp1 is critical for hepatic recovery from ER stress. Significance: We implicate Xbp1 in mediating the pro-survival response of the UPR.

AB - Background: The unfolded protein response (UPR) either restores homeostasis or promotes apoptosis in response to endoplasmic reticulum (ER) stress. Results: ER stress causes prolonged UPR activation, severe liver injury, and enhanced apoptosis in mice lacking hepatic Xbp1. Conclusion: Hepatic Xbp1 is critical for hepatic recovery from ER stress. Significance: We implicate Xbp1 in mediating the pro-survival response of the UPR.

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Hepatic Xbp1 gene deletion promotes endoplasmic reticulum stress-induced liver injury and apoptosis

Abstract

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