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Mol Cell ; 82(19): 3661-3676.e8, 2022 10 06.
Artículo en Inglés | MEDLINE | ID: mdl-36206740

RESUMEN

Mitochondrial Ca2+ uptake, mediated by the mitochondrial Ca2+ uniporter, regulates oxidative phosphorylation, apoptosis, and intracellular Ca2+ signaling. Previous studies suggest that non-neuronal uniporters are exclusively regulated by a MICU1-MICU2 heterodimer. Here, we show that skeletal-muscle and kidney uniporters also complex with a MICU1-MICU1 homodimer and that human/mouse cardiac uniporters are largely devoid of MICUs. Cells employ protein-importation machineries to fine-tune the relative abundance of MICU1 homo- and heterodimers and utilize a conserved MICU intersubunit disulfide to protect properly assembled dimers from proteolysis by YME1L1. Using the MICU1 homodimer or removing MICU1 allows mitochondria to more readily take up Ca2+ so that cells can produce more ATP in response to intracellular Ca2+ transients. However, the trade-off is elevated ROS, impaired basal metabolism, and higher susceptibility to death. These results provide mechanistic insights into how tissues can manipulate mitochondrial Ca2+ uptake properties to support their unique physiological functions.


Asunto(s)
Proteínas de Unión al Calcio/metabolismo , Calcio , Proteínas de Transporte de Catión/metabolismo , Proteínas de Transporte de Membrana Mitocondrial/metabolismo , Adenosina Trifosfato , Animales , Calcio/metabolismo , Canales de Calcio , Proteínas de Unión al Calcio/genética , Disulfuros/metabolismo , Humanos , Ratones , Proteínas de Transporte de Membrana Mitocondrial/genética , Especies Reactivas de Oxígeno/metabolismo
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