Mitochondrial sodium-calcium exchange—Can TMEM65 do it alone?
Authors:
- 7 October 2025
- journal article
- editorial
- Published by Elsevier in Cell Metabolism
- Vol. 37 (10) , 1927-1928
Abstract
No abstract availableKeywords
Funding Information
- National Institute of Neurological Disorders and Stroke
- American Heart Association
- National Heart, Lung, and Blood Institute
This publication has 9 references indexed in Scilit:
- TMEM65-dependent Ca2+ extrusion safeguards mitochondrial homeostasisNature Communications, 2025
- TMEM65 functions as the mitochondrial Na+/Ca2+ exchangerNature Cell Biology, 2025
- TMEM65 regulates and is required for NCLX-dependent mitochondrial calcium effluxNature Metabolism, 2025
- Mitochondrial signal transductionCell Metabolism, 2022
- Mitochondrial calcium exchange in physiology and diseasePhysiological Reviews, 2022
- The mitochondrial Na+/Ca2+ exchanger is essential for Ca2+ homeostasis and viabilityNature, 2017
- Integrative genomics identifies MCU as an essential component of the mitochondrial calcium uniporterNature, 2011
- A forty-kilodalton protein of the inner membrane is the mitochondrial calcium uniporterNature, 2011
- NCLX is an essential component of mitochondrial Na+/Ca2+exchangeProceedings of the National Academy of Sciences, 2009