Premium
Intracellular calcium release is required for caspase‐3 and ‐9 activation
Author(s) -
Tantral Lee,
Malathi Krishnamurthy,
Kohyama Shinya,
Silane Michael,
Berenstein Alejandro,
Jayaraman Thottala
Publication year - 2003
Publication title -
cell biochemistry and function
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.933
H-Index - 61
eISSN - 1099-0844
pISSN - 0263-6484
DOI - 10.1002/cbf.1050
Subject(s) - intracellular , calcium in biology , calcium , microbiology and biotechnology , chemistry , biophysics , pharmacology , biochemistry , biology , organic chemistry
Increase in intracellular Ca 2+ [Ca 2+ ]i regulates many biological functions including apoptosis, but the protein(s) linking [Ca 2+ ]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 Ca 2+ 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 Ca 2+ release plays a critical role in regulating the activity of caspases‐3 and ‐9 independent of Bcl‐2. Copyright © 2003 John Wiley & Sons, Ltd.