ATP synthase K+- and H+-flux drive ATP synthesis and enable mitochondrial K+-uniporter functionстатья

Дата последнего поиска статьи во внешних источниках: 11 апреля 2019 г.

Работа с статьей


[1] Atp synthase k+- and h+-flux drive atp synthesis and enable mitochondrial k+-uniporter function / J. Magdalena, K. Evgeny, D. B. Zorov et al. // bioRxiv (The preprint server for biology). — 2018. — P. 1–33. 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. [ DOI ]

Публикация в формате сохранить в файл сохранить в файл сохранить в файл сохранить в файл сохранить в файл сохранить в файл скрыть