Succinate dehydrogenase deficiency in a chromaffin cell model retains metabolic fitness through the maintenance of mitochondrial NADH oxidoreductase function
Author:
Affiliation:
1. Institute of Metabolism and Systems Research, College of Medical and Dental Sciences University of Birmingham Birmingham UK
2. Université de Paris, PARCC, INSERM, Equipe Labellisée par la Ligue contre le Cancer Paris France
Funder
Wellcome Trust
Cancer Research UK
Publisher
Wiley
Subject
Genetics,Molecular Biology,Biochemistry,Biotechnology
Link
https://onlinelibrary.wiley.com/doi/pdf/10.1096/fj.201901456R
Reference27 articles.
1. SDH mutations in cancer
2. SDH Mutations Establish a Hypermethylator Phenotype in Paraganglioma
3. Succinate links TCA cycle dysfunction to oncogenesis by inhibiting HIF-α prolyl hydroxylase
4. Mutations in SDHD , a Mitochondrial Complex II Gene, in Hereditary Paraganglioma
5. Mutation of a nuclear succinate dehydrogenase gene results in mitochondrial respiratory chain deficiency
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