Defective NADPH production in mitochondrial disease complex I causes inflammation and cell death

Eduardo Balsa; Elizabeth A. Perry; Christopher F. Bennett; Mark Jedrychowski; Steven P. Gygi; John G. Doench; Pere Puigserver

doi:10.1038/s41467-020-16423-1

Nature Communications (Jun 2020)

Defective NADPH production in mitochondrial disease complex I causes inflammation and cell death

Eduardo Balsa,
Elizabeth A. Perry,
Christopher F. Bennett,
Mark Jedrychowski,
Steven P. Gygi,
John G. Doench,
Pere Puigserver

Affiliations

Eduardo Balsa: Department of Cancer Biology, Dana-Farber Cancer Institute
Elizabeth A. Perry: Department of Cancer Biology, Dana-Farber Cancer Institute
Christopher F. Bennett: Department of Cancer Biology, Dana-Farber Cancer Institute
Mark Jedrychowski: Department of Cell Biology, Harvard Medical School
Steven P. Gygi: Department of Cell Biology, Harvard Medical School
John G. Doench: Broad Institute of MIT and Harvard
Pere Puigserver: Department of Cancer Biology, Dana-Farber Cancer Institute

DOI: https://doi.org/10.1038/s41467-020-16423-1
Journal volume & issue: Vol. 11, no. 1
pp. 1 – 12

Abstract

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Mitochondrial oxidative phosphorylation produces ATP and is an important source for cellular energy equivalents. Here the authors perform a cell-based screen to identify genes that alleviate perturbed mitochondrial complex I function and identify malic enzyme (ME-1), which promotes survival by production of NADPH and glutathione.

Published in Nature Communications

ISSN: 2041-1723 (Online)
Publisher: Nature Portfolio
Country of publisher: United Kingdom
LCC subjects: Science
Website: https://www.nature.com/ncomms/

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