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Nature|June 21, 2011
Integrative genomics identifies MCU as an essential component of the mitochondrial calcium uniporterJoshua M Baughman, Fabiana Perocchi, Hany S Girgis, et al.Science (New York, N.Y.)|February 27, 2016
Hypoxia as a therapy for mitochondrial diseaseIsha H Jain, Luca Zazzeron, Rahul Goli, et al.American Journal of Physiology. Lung Cellular and Molecular Physiology|December 7, 2018
Impaired hypoxic pulmonary vasoconstriction in a mouse model of Leigh syndromeGrigorij Schleifer, Eizo Marutani, Michele Ferrari, et al.Journal of Cell Science|November 5, 2002
Defects in keratinocyte activation during wound healing in the syndecan-1-deficient mouseMary Ann Stepp, Heather E Gibson, Purvi H Gala, et al.Science (New York, N.Y.)|November 16, 2013
EMRE is an essential component of the mitochondrial calcium uniporter complexYasemin Sancak, Andrew L Markhard, Toshimori Kitami, et al.Cell Metabolism|August 13, 2019
Leigh Syndrome Mouse Model Can Be Rescued by Interventions that Normalize Brain Hyperoxia, but Not HIF ActivationIsha H Jain, Luca Zazzeron, Olga Goldberger, et al.Elife|June 17, 2016
Mitochondrial dysfunction remodels one-carbon metabolism in human cellsXiaoyan Robert Bao, Shao-En Ong, Olga Goldberger, et al.Nature|May 29, 2020
Hepatic NADH reductive stress underlies common variation in metabolic traitsRussell P Goodman, Andrew L Markhard, Hardik Shah, et al.Molecular Genetics and Metabolism|March 23, 2021
Hypoxia ameliorates brain hyperoxia and NAD+ deficiency in a murine model of Leigh syndromeRobert M H Grange, Rohit Sharma, Hardik Shah, et al.Cell Metabolism|December 15, 2023
ChREBP is activated by reductive stress and mediates GCKR-associated metabolic traitsCharandeep Singh, Byungchang Jin, Nirajan Shrestha, et al.Pageof 2