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Article

UPR pathways combine to prevent hepatic steatosis caused by ER stress-mediated suppression of transcriptional master regulators.

Developmental cell - 1 Dec 2008

Rutkowski D Thomas, Wu Jun, Back Sung-Hoon, Callaghan Michael U, Ferris Sean P, Iqbal Jahangir, Clark Robert, Miao Hongzhi, Hassler Justin R, Fornek Jamie, Katze Michael G, Hussain M Mahmood, Song Benbo, Swathirajan Jayanth, Wang Junying, Yau Grace D-Y, Kaufman Randal J

Abstract excerpt

The unfolded protein response (UPR) is linked to metabolic dysfunction, yet it is not known how endoplasmic reticulum (ER) disruption might influence metabolic pathways. Using a multilayered genetic approach, we find that mice with genetic ablations of either ER stress-sensing pathways (ATF6alpha, eIF2alpha, IRE1alpha) or of ER quality control (p58(IPK)) share a common dysregulated response to ER stress that...

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Share to Carcinoma, Hepatocellular
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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Identifiers

PMID: 19081072
DOI: 10.1016/j.devcel.2008.10.015
PMCID: PMC2923556

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