Journal
CELL CALCIUM
Volume 74, Issue -, Pages 86-93Publisher
ELSEVIER SCI LTD
DOI: 10.1016/j.ceca.2018.06.006
Keywords
Mitochondria; Calcium; Oxidants; MCU; MICU1; MCUR1; EMRE; MCUb; SLC25A23; Channel; MiST; Miro1; Magnesium
Categories
Funding
- NIH [R01GM109882, R01HL086699, R01HL119306, 1S10RR027327]
- AHA fellowship [17PRE33660720]
- NIH K99/R00 grant [1K99HL138268-01]
- NATIONAL CENTER FOR RESEARCH RESOURCES [S10RR027327] Funding Source: NIH RePORTER
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL119306, R01HL086699, K99HL138268] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [R01GM109882] Funding Source: NIH RePORTER
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Ca2+ flux across the inner mitochondrial membrane (IMM) regulates cellular bioenergetics, intra-cellular cytoplasmic Ca2+ signals, and various cell death pathways. Ca2+ entry into the mitochondria occurs due to the highly negative membrane potential (Delta psi(m)) through a selective inward rectifying MCU channel. In addition to being regulated by various mitochondrial matrix resident proteins such as MICUs, MCUb, MCUR1 and EMRE, the channel is transcriptionally regulated by upstream Ca2+ cascade, post transnational modification and by divalent cations. The mode of regulation either inhibits or enhances MCU channel activity and thus regulates mitochondrial metabolism and cell fate.
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