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Endoplasmic Reticulum Stress and Glycogen Synthase Kinase-3β Activation in Apolipoprotein E–Deficient Mouse Models of Accelerated Atherosclerosis
Author(s) -
Cameron S. McAlpine,
Anna J. Bowes,
Mohammad I. Khan,
Yuanyuan Shi,
Geoff H. Werstuck
Publication year - 2011
Publication title -
arteriosclerosis thrombosis and vascular biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.007
H-Index - 270
eISSN - 1524-4636
pISSN - 1079-5642
DOI - 10.1161/atvbaha.111.237941
Subject(s) - endoplasmic reticulum , gsk 3 , glycogen synthase , unfolded protein response , apolipoprotein b , chemistry , glycogen , kinase , medicine , microbiology and biotechnology , endocrinology , biology , cholesterol
The goal of this study was to examine the role of endoplasmic reticulum (ER) stress signaling and the contribution of glycogen synthase kinase (GSK)-3β activation in hyperglycemic, hyperhomocysteinemic, and high-fat-fed apolipoprotein E-deficient (apoE(-/-)) mouse models of accelerated atherosclerosis.

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