Authors: Daniel Bakowski Charmaine Nelson Anant B Parekh
Publish Date: 2012/03/14
Volume: 464, Issue: 1, Pages: 27-32
Abstract
Plasma membrane storeoperated Ca2+ releaseactivated Ca2+ CRAC channels are a widespread and conserved Ca2+ influx pathway driving activation of a range of spatially and temporally distinct cellular responses Although CRAC channels are activated by the loss of Ca2+ from the endoplasmic reticulum their gating is regulated by mitochondria Through their ability to buffer cytoplasmic Ca2+ mitochondria take up Ca2+ released from the endoplasmic reticulum by InsP3 receptors leading to more extensive store depletion and stronger activation of CRAC channels Mitochondria also buffer Ca2+ that enters through CRAC channels reducing Ca2+dependent slow inactivation of the channels In addition depolarised mitochondria impair movement of the CRAC channel activating protein STIM1 across the endoplasmic reticulum membrane Because they regulate CRAC channel activity particularly Ca2+dependent slow inactivation mitochondria influence CRAC channeldriven enzyme activation secretion and gene expression Mitochondrial regulation of CRAC channels therefore provides an important control element to the regulation of intracellular Ca2+ signalling
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