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10.1038/s41419-017-0179-0

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


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pmid29491433
      Cell+Death+Dis 2018 ; 9 (3 ): 334
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  • Emerging molecular mechanisms in chemotherapy: Ca(2+) 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[Feb]; 9 (3 ): 334 PMID29491433 show ga
  • Inter-organellar communication often takes the form of Ca(2+) signals. These Ca(2+) signals originate from the endoplasmic reticulum (ER) and regulate different cellular processes like metabolism, fertilization, migration, and cell fate. A prime target for Ca(2+) signals are the mitochondria. ER-mitochondrial Ca(2+) 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 Ca(2+) concentrations are manifold higher than in the cytosol, allowing for rapid mitochondrial Ca(2+) uptake. In the mitochondria, the Ca(2+) signal is decoded differentially depending on its spatiotemporal characteristics. While Ca(2+) oscillations stimulate metabolism and constitute pro-survival signaling, mitochondrial Ca(2+) overload results in apoptosis. Many chemotherapeutics depend on efficient ER-mitochondrial Ca(2+) signaling to exert their function. However, several oncogenes and tumor suppressors present in the MAMs can alter Ca(2+) signaling in cancer cells, rendering chemotherapeutics ineffective. In this review, we will discuss recent studies that connect ER-mitochondrial Ca(2+) transfer, tumor suppressors and oncogenes at the MAMs, and chemotherapy.
  • |*Calcium Signaling [MESH]
  • |Animals [MESH]
  • |Antineoplastic Agents/*metabolism/therapeutic use [MESH]
  • |Calcium/metabolism [MESH]
  • |Endoplasmic Reticulum/genetics/*metabolism [MESH]
  • |Humans [MESH]
  • |Mitochondria/genetics/*metabolism [MESH]
  • |Mitochondrial Membranes/*metabolism [MESH]


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