Autor: |
Lee Tantral, Krishnamurthy Malathi, Shinya Kohyama, Michael Silane, Alejandro Berenstein |
Předmět: |
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Zdroj: |
Cell Biochemistry & Function; January/February2004, Vol. 22 Issue 1, p35-40, 6p |
Abstrakt: |
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 © 2003 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR] |
Databáze: |
Complementary Index |
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