Intracellular calcium release is required for caspase-3 and-9 activation

被引：50

作者：

Tantral, L

Malathi, K

Kohyama, S

Silane, M

Berenstein, A

Jayaraman, T

机构：

[1] St Lukes Roosevelt Hosp, Vasc Biol Lab, Dept Med, New York, NY 10025 USA

[2] Beth Israel Deaconess Med Ctr, Div Vasc Surg, New York, NY 10003 USA

[3] Beth Israel Deaconess Med Ctr, Div Endovasc Surg, New York, NY 10003 USA

[4] Columbia Univ, Coll Phys & Surg, Dept Med, Div Cardiol, New York, NY USA

来源：

CELL BIOCHEMISTRY AND FUNCTION | 2004年 / 22卷 / 01期

关键词：

calcium; caspases; IP3; apoptosis; lymphocytes;

D O I：

10.1002/cbf.1050

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

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.

引用

页码：35 / 40

页数：6

共 20 条

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