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Oncogene 2008 Oct;27(50):6419-33

Department of Biochemistry, McIntyre Medical Sciences Building, McGill University, Montreal, Quebec, Canada.

Apoptosis is essential for normal development and maintenance of homeostasis, and disruption of apoptotic pathways is associated with multiple disease states, including cancer. Although initially identified as central regulators of apoptosis at the level of mitochondria, an important role for BCL-2 proteins at the endoplasmic reticulum is now well established. Signaling pathways emanating from the endoplasmic reticulum (ER) are involved in apoptosis initiated by stimuli as diverse as ER stress, oncogene expression, death receptor (DR) ligation and oxidative stress, and the BCL-2 family is almost invariably implicated in the regulation of these pathways. Read More

Diabetes 2009 Feb 25;58(2):422-32. Epub 2008 Nov 25.

Department of Cellular and Physiological Sciences, University of British Columbia, Vancouver, British Comlumbia, Canada.

Objective: Endoplasmic reticulum (ER) stress has been implicated in the pathogenesis of diabetes, but the roles of specific ER Ca(2+) release channels in the ER stress-associated apoptosis pathway remain unknown. Here, we examined the effects of stimulating or inhibiting the ER-resident inositol trisphosphate receptors (IP(3)Rs) and the ryanodine receptors (RyRs) on the induction of beta-cell ER stress and apoptosis.

Research Design And Methods: Kinetics of beta-cell death were tracked by imaging propidium iodide incorporation and caspase-3 activity in real time. Read More

Mol Pharmacol 2006 Oct 18;70(4):1424-34. Epub 2006 Jul 18.

Arthritis and Immune Disorder Research Centre, University Health Network and Department of Immunology, University of Toronto, Medical Discovery Tower, 8th Floor, Rm 8-356, 101 College St., Toronto, ON, Canada M5G 1L7.

Disturbances of endoplasmic reticulum (ER) Ca2+ homeostasis or protein processing can lead to ER stress-induced cell death. Increasing evidence suggests that oxidative stress (OS) plays an important role in a variety of cell death mechanisms. To investigate the role of OS in ER stress, we measured OS in response to three ER stress agents: econazole (Ec), which stimulates ER Ca2+ release and blocks Ca2+ influx; thapsigargin (Tg), a sarco(endo)plasmic reticulum Ca2+ ATPase inhibitor that releases ER Ca2+ and stimulates Ca2+ influx; and tunicamycin (Tu), a glycosylation inhibitor that causes protein accumulation in the ER. Read More

Vitam Horm 2004 ;67:169-88

Department of Pharmacology State University of New York Upstate Medical University Syracuse, New York 13210, USA.

Calcium (Ca(2+)) is one of the highly versatile second messengers critical in cellular pathophysiology. Alterations in Ca(2+) homeostasis affect many cellular processes, including apoptosis. Recent studies have started to unravel the molecular mechanisms of apoptosis regulation in context to intracellular Ca(2+) pools. Read More