Calnexin Silencing in Mouse Neonatal Cardiomyocytes Induces Ca2+Cycling Defects, ER Stress, and Apoptosis
Author:
Affiliation:
1. Department of Physiology; University of Toronto; Toronto Ontario Canada
2. Heart and Stroke/Richard Lewar Centre of Excellence; University of Toronto; Toronto Ontario Canada
Publisher
Wiley
Subject
Cell Biology,Clinical Biochemistry,Physiology
Reference26 articles.
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3. Potent lectin-independent chaperone function of calnexin under conditions prevalent within the lumen of the endoplasmic reticulum;Brockmeier;Biochemistry,2006
4. Ca2+ influx-induced sarcoplasmic reticulum Ca2+ overload causes mitochondrial-dependent apoptosis in ventricular myocytes;Chen;Circ Res,2005
5. Endoplasmic reticulum stress in the absence of calnexin;Coe;Cell Stress Chaperones,2008
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