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