Mitochondrial calcium uniporter stabilization preserves energetic homeostasis during Complex I impairment
Mitochondrial complex I deficiency is frequent in congenital, neurologic and cardiovascular disease. Here the authors demonstrate that Complex I stimulates the turnover of a mitochondrial calcium channel, which becomes stabilized during Complex I deficiency, preserving energetic homeostasis.
Main Authors: | Enrique Balderas, David R. Eberhardt, Sandra Lee, John M. Pleinis, Salah Sommakia, Anthony M. Balynas, Xue Yin, Mitchell C. Parker, Colin T. Maguire, Scott Cho, Marta W. Szulik, Anna Bakhtina, Ryan D. Bia, Marisa W. Friederich, Timothy M. Locke, Johan L. K. Van Hove, Stavros G. Drakos, Yasemin Sancak, Martin Tristani-Firouzi, Sarah Franklin, Aylin R. Rodan, Dipayan Chaudhuri |
---|---|
Format: | Article |
Language: | English |
Published: |
Nature Portfolio
2022-05-01
|
Series: | Nature Communications |
Online Access: | https://doi.org/10.1038/s41467-022-30236-4 |
Similar Items
-
Author Correction: Mitochondrial calcium uniporter stabilization preserves energetic homeostasis during Complex I impairment
by: Enrique Balderas, et al.
Published: (2022-06-01) -
Exploring the In Vivo Role of the Mitochondrial Calcium Uniporter in Brown Fat Bioenergetics
by: Daniel Flicker, et al.
Published: (2019-04-01) -
MCU encodes the pore conducting mitochondrial calcium currents
by: Dipayan Chaudhuri, et al.
Published: (2013-06-01) -
Uniportal Endoscopic Lumbar Interbody Fusion
by: Ralf Wagner, et al.
Published: (2020-07-01) -
The mechanism of MICU-dependent gating of the mitochondrial Ca2+uniporter
by: Vivek Garg, et al.
Published: (2021-08-01)