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ATP synthase K+- and H+-flux drive ATP synthesis and enable mitochondrial K+-uniporter functionстатья
- Авторы: Magdalena Juhaszova, Evgeny Kobrinsky, Zorov Dmitry B., Bradley Nuss H., Yael Yaniv, Fishbein Kenneth W., de Cabo Rafael, Lluis Montoliu, Gabelli Sandra B., Aon Miguel A., Sonia Cortassa, Sollott Steven J.
- Журнал: bioRxiv (The preprint server for biology)
- Год издания: 2018
- Первая страница: 1
- Последняя страница: 33
- DOI: 10.1101/355776
- Аннотация: We show that mammalian ATP synthase (F1Fo) utilizes the ion gradient energy not only of H+ but also of K+ to make ATP with the relative permeability of H+:K+ at ~106:1. F1Fo can be upregulated to increase the total ion-flux (at constant H+:K+) against a constant load without slip or leak, via the IF1-mediated increase in chemo-mechanical efficiency of F1Fo regulated by endogenous survival-related proteins, Bcl-xL and Mcl-1, and synthetic small molecules, diazoxide and pinacidil. Increasing ATP synthesis driven by K+ - and H+-influx through Fo provides a simple way for F1Fo to operate as a primary mitochondrial K+-uniporter to regulate matrix osmotic balance matching metabolic energy supply with demand. This essential mitochondrial homeostatic mechanism also enables F1Fo to function as a recruitable mitochondrial KATP-channel, whereby triggered increases of mitochondrial K+-influx and matrix-volume upregulate the signal cascade resulting in desensitization of the permeability transition pore, enhancing cell survival during ischemia-reperfusion injury.
- Добавил в систему: Зоров Дмитрий Бориcович