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The Role of Mitochondria in the Activation/Maintenance of SOCE: Membrane Contact Sites as Signaling Hubs Sustaining Store-Operated Ca2+ Entry

Published inAdvances in Experimental Medicine and Biology, vol. 993, p. 277-296
Publication date2017
Abstract

Store-operated Ca2+ entry (SOCE) is a cell signaling pathway essential for immune and muscle function controlled by dynamic interactions between Ca2+-sensing STIM proteins on the endoplasmic reticulum (ER) and Ca2+-permeable ORAI channels on the plasma membrane (PM). STIM-ORAI interactions occur at membrane contact sites (MCS), evolutionarily conserved cellular structures characterized by the close apposition (10-20 nm) between the ER and target membranes that facilitate the exchange of lipids by non-vesicular transport mechanisms. STIM-ORAI interactions were considered to be restricted to ER-PM MCS, but recent evidence indicates that productive interactions take place between ER-bound STIM1 and Ca2+ channels located in intracellular organelles. Interactions between the ER and endosomes or lysosomes regulate the lipid homeostasis of these organelles and the propagation of Ca2+ signals initiated by the release of Ca2+ from acidic stores. Intracellular MCS also regulate the efficiency of phagocytosis, a fundamental cellular process essential for immunity and tissue homeostasis, by ensuring the coordinated opening of Ca2+ channels on phagocytic vacuoles and of Ca2+ release channels on juxtaposed ER stores. In this chapter, we review the current knowledge on the molecular composition and architecture of membrane contact sites that sustain Ca2+ signals at the plasma membrane and in intracellular organelles.

Keywords
  • Calcium
  • Ion channels
  • Contact sites
Citation (ISO format)
DEMAUREX, Nicolas, GUIDO, Danièle. The Role of Mitochondria in the Activation/Maintenance of SOCE: Membrane Contact Sites as Signaling Hubs Sustaining Store-Operated Ca2+ Entry. In: Advances in Experimental Medicine and Biology, 2017, vol. 993, p. 277–296. doi: 10.1007/978-3-319-57732-6_15
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ISSN of the journal0065-2598
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