Abstract
An important function of mitochondria is to shape cytosolic Ca2+ signals by taking up and subsequently releasing Ca2+ ions. Ca2+ sequestration by mitochondria decreases the local Ca2+ concentration in the vicinity of Ca2+ entry channels, a process thought to underlie the modulation of store-operated Ca2+ entry (SOCE) by mitochondria. Early studies showed that Ca2+ elevations in the vicinity of SOCE channels exert a negative feedback on the current amplitude, causing a slow Ca2+ -dependent inactivation that is prevented by respiring mitochondria. Local buffering of Ca2+ by mitochondria, however, implies a close proximity between mitochondria and SOCE channels that appears at odds with recent morphological and functional evidence showing that SOCE activation relies on the close apposition of thin cortical ER sheets and the docking of STIM1 ER proteins to plasma membrane Orai or TRP channels. In this chapter, we review the recently identified mitochondrial channels and exchangers that are thought to mediate the fluxes of Ca2+ across mitochondria, and re-evaluate the role of mitochondria as SOCE modulators in view of our recent knowledge about the machinery leading to SOCE.
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Demaurex, N., Frieden, M. (2012). The Role of Mitochondria in the Activation/Maintenance of SOCE. In: Groschner, K., Graier, W., Romanin, C. (eds) Store-operated Ca2+ entry (SOCE) pathways. Springer, Vienna. https://doi.org/10.1007/978-3-7091-0962-5_14
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