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

Shantel Olivares, Anne S. Henkel*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

23 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 languageEnglish (US)
Pages (from-to)30142-30151
Number of pages10
JournalJournal of Biological Chemistry
Volume290
Issue number50
DOIs
StatePublished - Dec 11 2015

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Cell Biology

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