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Updated: Jul 20, 2026

F1FO ATPase Vesicle Preparation and Technique for Performing Patch Clamp Recordings of Submitochondrial Vesicle Membranes
Published on: May 4, 2013
ATP from subplasmalemmal mitochondria controls Ca2+-dependent inactivation of CRAC channels
Gema B Montalvo1, Antonio R Artalejo, Juan A Gilabert
1Department 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.
Abstract:
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.
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