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• W1981642705 abstract "A recently studied endoplasmic reticulum (ER) stress regulator, Bax inhibitor-1 (BI-1) plays a regulatory role in mitochondrial Ca2+ levels. In this study, we identified ER-resident and mitochondria-associated ER membrane (MAM)-resident populations of BI-1. ER stress increased mitochondrial Ca2+ to a lesser extent in BI-1–overexpressing cells (HT1080/BI-1) than in control cells, most likely as a result of impaired mitochondrial Ca2+ intake ability and lower basal levels of intra-ER Ca2+. Moreover, opening of the Ca2+-induced mitochondrial permeability transition pore (PTP) and cytochrome c release were regulated by BI-1. In HT1080/BI-1, the basal mitochondrial membrane potential was low and also resistant to Ca2+ compared with control cells. The activity of the mitochondrial membrane potential-dependent mitochondrial Ca2+ intake pore, the Ca2+ uniporter, was reduced in the presence of BI-1. This study also showed that instead of Ca2+, other cations including K+ enter the mitochondria of HT1080/BI-1 through mitochondrial Ca2+-dependent ion channels, providing a possible mechanism by which mitochondrial Ca2+ intake is reduced, leading to cell protection. We propose a model in which BI-1–mediated sequential regulation of the mitochondrial Ca2+ uniporter and Ca2+-dependent K+ channel opening inhibits mitochondrial Ca2+ intake, thereby inhibiting PTP function and leading to cell protection." @default.
• W1981642705 created "2016-06-24" @default.
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• W1981642705 date "2014-06-05" @default.
• W1981642705 modified "2023-09-26" @default.
• W1981642705 title "Bax Inhibitor-1-Mediated Inhibition of Mitochondrial Ca2+ Intake Regulates Mitochondrial Permeability Transition Pore Opening and Cell Death" @default.
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• W1981642705 doi "https://doi.org/10.1038/srep05194" @default.
• W1981642705 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4046133" @default.
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