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J. Biol. Chem., Vol. 281, Issue 47, 35616-35623, November 24, 2006

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ATP from Subplasmalemmal Mitochondria Controls Ca²⁺-dependent Inactivation of CRAC Channels^*

From the Department of Toxicology and Pharmacology, Instituto de Farmacología y Toxicología, Facultad de Veterinaria, Universidad Complutense de Madrid, Avenida Puerta de Hierro, s/n. 28040 Madrid, Spain

A sustained Ca²⁺ entry is the primary signal for T lymphocyte activation after antigen recognition. This Ca²⁺ entry mainly occurs through store-operated Ca²⁺ channels responsible for a highly selective Ca²⁺ current known as I_CRAC. Ca²⁺ ions act as negative feedback regulators of I_CRAC, promoting its inactivation. Mitochondria, which act as intracellular Ca²⁺ buffers, have been proposed to control all stages of CRAC current and, hence, intracellular Ca²⁺ signaling in several types of non-excitable cells. Using the whole-cell configuration of the patch clamp technique, which allows control of the intracellular environment, we report here that respiring mitochondria located close to CRAC channels can regulate slow Ca²⁺-dependent inactivation of I_CRAC by increasing the Ca²⁺-buffering capacity beneath the plasma membrane, mainly through the release of ATP.

Received for publication, April 12, 2006 , and in revised form, September 6, 2006.

^* This work was supported by DGICYT Grants BFI-2002-01101 (to J. A. G.) and BFU-2005-06034 (to A. R. A.), CAM Grant GR/SAL/0522/2004 (to J. A. G.), and UCM-CAM Grant PR45/05-14162 (to J. A. G.). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ FPI predoctoral fellow from the Spanish Education and Science Ministry.

² Researcher of the Ramón y Cajal Programme. To whom correspondence should be addressed. Tel.: 34-91-394-4036; Fax: 34-91-394-3851; E-mail: jagilabe{at}vet.ucm.es.

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