Heteroplasmic mutations of the mitochondrial genome cause paradoxical effects on mitochondrial functions

FASEB Journal

Volumn 26, Issue 12, 2012, Pages 4914-4924

  Zhang, Chengkang ^a   Huang, Vincent H ^a   Simon, Mariella ^b   Sharma, Lokendra K ^c   Fan, Weiwei ^d   Haas, Richard ^a,e,f   Wallace, Douglas C ^g,h   Bai, Yidong ^c   Huang, Taosheng ^a,b  

^a UNIVERSITY OF CALIFORNIA   (United States)

^b UNIVERSITY OF CALIFORNIA   (United States)

^c Mays Cancer Center at UT Health San Antonio   (United States)

^d SALK INSTITUTE FOR BIOLOGICAL STUDIES   (United States)

^e UNIVERSITY OF CALIFORNIA   (United States)

^f UNIVERSITY OF CALIFORNIA SAN DIEGO   (United States)

^g UNIVERSITY OF PENNSYLVANIA   (United States)

^h CHILDREN S HOSPITAL OF PHILADELPHIA   (United States)

Author keywords

Cybrid; ND2; Nutrients

Indexed keywords

MITOCHONDRIAL DNA; REACTIVE OXYGEN METABOLITE;

ADULT; ANAEROBIC GLYCOLYSIS; APOPTOSIS; ARTICLE; CARCINOGENESIS; CELL FRACTIONATION; CELL GROWTH; CELL RESPIRATION; CELL VIABILITY; DISORDERS OF MITOCHONDRIAL FUNCTIONS; FEMALE; GENE MUTATION; GENOTYPE ENVIRONMENT INTERACTION; HETEROPLASMY; HUMAN; HUMAN CELL; MALE; MITOCHONDRIAL GENOME; OXIDATIVE PHOSPHORYLATION; OXYGEN CONSUMPTION; PHENOTYPE; PRIORITY JOURNAL;

ADENOSINE TRIPHOSPHATASES; ADULT; APOPTOSIS; CARRIER PROTEINS; CELL PROLIFERATION; CELLS, CULTURED; ELECTRON TRANSPORT COMPLEX I; GALACTOSE; GENOME, MITOCHONDRIAL; HUMANS; HYBRID CELLS; MALE; MEMBRANE PROTEINS; MITOCHONDRIA; MITOCHONDRIAL DISEASES; OXIDATIVE PHOSPHORYLATION; OXYGEN CONSUMPTION; POINT MUTATION; REACTIVE OXYGEN SPECIES;

EID: 84870377032     PISSN: None     EISSN: 15306860     Source Type: Journal    
DOI: 10.1096/fj.12-206532     Document Type: Article

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