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SHR Neuro Krebs Kardio Lipid

Malli, R; Graier, WF.
The Role of Mitochondria in the Activation/Maintenance of SOCE: The Contribution of Mitochondrial Ca(2+) Uptake, Mitochondrial Motility, and Location to Store-Operated Ca(2+) Entry.
Adv Exp Med Biol. 2017; 993: 297-319.
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Autor/innen der Med Uni Graz:
Graier Wolfgang
Malli Roland

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Plum Analytics:
In most cell types, the depletion of internal Ca(2+) stores triggers the activation of Ca(2+) entry. This crucial phenomenon is known since the 1980s and referred to as store-operated Ca(2+) entry (SOCE). With the discoveries of the stromal-interacting molecules (STIMs) and the Ca(2+)-permeable Orai channels as the long-awaited molecular constituents of SOCE, the role of mitochondria in controlling the activity of this particular Ca(2+) entry pathway is kind of buried in oblivion. However, the capability of mitochondria to locally sequester Ca(2+) at sites of Ca(2+) release and entry was initially supposed to rule SOCE by facilitating the Ca(2+) depletion of the endoplasmic reticulum and removing entering Ca(2+) from the Ca(2+)-inhibitable channels, respectively. Moreover, the central role of these organelles in controlling the cellular energy metabolism has been linked to the activity of SOCE. Nevertheless, the exact molecular mechanisms by which mitochondria actually determine SOCE are still pretty obscure. In this essay we describe the complexity of the mitochondrial Ca(2+) uptake machinery and its regulation, molecular components, and properties, which open new ways for scrutinizing the contribution of mitochondria to SOCE. Moreover, data concerning the variability of the morphology and cellular distribution of mitochondria as putative determinants of SOCE activation, maintenance, and termination are summarized.

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