TGF β1 induces prolonged mitochondrial ROS generation through decreased complex IV activity with senescent arrest in Mv1Lu cells

Oncogene

Volumn 24, Issue 11, 2005, Pages 1895-1903

  Yoon, Young Sil ^a   Lee, Jae Ho ^a   Hwang, Sung Chul ^a   Choi, Kyeong Sook ^a   Yoon, Gyesoon ^a  

^a Ajou University School of Medicine   (South Korea)

Author keywords

Complex IV defect; Mitochondrial dysfunction; Reactive oxygen species; Senescence; TGF 1

Indexed keywords

CYTOCHROME C OXIDASE; REACTIVE OXYGEN METABOLITE; TRANSFORMING GROWTH FACTOR BETA; TRANSFORMING GROWTH FACTOR BETA1;

ANIMAL CELL; APOPTOSIS; ARTICLE; CELL CYCLE; CELL CYCLE G1 PHASE; CELL GROWTH; CELL PROTECTION; CONTROLLED STUDY; ENZYME ACTIVITY; EPITHELIUM CELL; IN VIVO STUDY; MEMBRANE POTENTIAL; MITOCHONDRIAL MEMBRANE; MITOCHONDRIAL RESPIRATION; MITOCHONDRION; NONHUMAN; PHENOTYPE; PRIORITY JOURNAL; PROTEIN FUNCTION; PROTEIN PROTEIN INTERACTION; SENESCENCE; ANIMAL; CELL AGING; CELL LINE; DRUG EFFECT; ENZYMOLOGY; LUNG; METABOLISM; OXYGEN CONSUMPTION; PHYSIOLOGY; RESPIRATORY TRACT MUCOSA;

ANIMALS; CELL AGING; CELL LINE; ELECTRON TRANSPORT COMPLEX IV; LUNG; MITOCHONDRIA; OXYGEN CONSUMPTION; REACTIVE OXYGEN SPECIES; RESPIRATORY MUCOSA; TRANSFORMING GROWTH FACTOR BETA; TRANSFORMING GROWTH FACTOR BETA1;

EID: 16244377705     PISSN: 09509232     EISSN: None     Source Type: Journal    
DOI: 10.1038/sj.onc.1208262     Document Type: Article

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