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10.1038/s41419-017-0179-0

http://scihub22266oqcxt.onion/10.1038/s41419-017-0179-0
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C5832420!5832420!29491433
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suck abstract from ncbi


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pmid29491433      Cell+Death+Dis 2018 ; 9 (3): ä
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  • Emerging molecular mechanisms in chemotherapy: Ca2+ signaling at the mitochondria-associated endoplasmic reticulum membranes #MMPMID29491433
  • Kerkhofs M; Bittremieux M; Morciano G; Giorgi C; Pinton P; Parys JB; Bultynck G
  • Cell Death Dis 2018[Mar]; 9 (3): ä PMID29491433show ga
  • Inter-organellar communication often takes the form of Ca2+ signals. These Ca2+ signals originate from the endoplasmic reticulum (ER) and regulate different cellular processes like metabolism, fertilization, migration, and cell fate. A prime target for Ca2+ signals are the mitochondria. ER?mitochondrial Ca2+ transfer is possible through the existence of mitochondria-associated ER membranes (MAMs), ER structures that are in the proximity of the mitochondria. This creates a micro-domain in which the Ca2+ concentrations are manifold higher than in the cytosol, allowing for rapid mitochondrial Ca2+ uptake. In the mitochondria, the Ca2+ signal is decoded differentially depending on its spatiotemporal characteristics. While Ca2+ oscillations stimulate metabolism and constitute pro-survival signaling, mitochondrial Ca2+ overload results in apoptosis. Many chemotherapeutics depend on efficient ER?mitochondrial Ca2+ signaling to exert their function. However, several oncogenes and tumor suppressors present in the MAMs can alter Ca2+ signaling in cancer cells, rendering chemotherapeutics ineffective. In this review, we will discuss recent studies that connect ER?mitochondrial Ca2+ transfer, tumor suppressors and oncogenes at the MAMs, and chemotherapy.
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