Journal
CELL BIOCHEMISTRY AND FUNCTION
Volume 22, Issue 1, Pages 35-40Publisher
WILEY
DOI: 10.1002/cbf.1050
Keywords
calcium; caspases; IP3; apoptosis; lymphocytes
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Funding
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R15AI089518] Funding Source: NIH RePORTER
- NIAID NIH HHS [R15 AI089518, R15 AI089518-01] Funding Source: Medline
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Increase in intracellular Ca2+ [Ca2+]i regulates many biological functions including apoptosis, but the protein(s) linking [Ca2+]i and apoptosis are not completely understood. We have previously shown that IP3R-deficient cells are resistant to T-cell receptor (TCR)-induced apoptosis due to lack of Ca2+ release from endoplasmic reticulum (ER) and calcineurin activation. Here we show that caspase-9 and -3 are not activated in IP3R-deficient cells after TCR stimulation, consistent with the resistance of these cells to apoptosis. However, we also demonstrate that Bcl-2 expression in IP3R-deficient cells is comparable to control cells. Taken together, these results strongly suggest that IP3R-mediated Ca2+ release plays a critical role in regulating the activity of caspases-3 and -9 independent of Bcl-2. Copyright (C) 2003 John Wiley Sons, Ltd.
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