期刊
JOURNAL OF BIOLOGICAL CHEMISTRY
卷 281, 期 47, 页码 35616-35623出版社
AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
DOI: 10.1074/jbc.M603518200
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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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