Loss of PINK1 causes mitochondrial functional defects and increased sensitivity to oxidative stress

Proceedings of the National Academy of Sciences of the United States of America

Volumn 105, Issue 32, 2008, Pages 11364-11369

  Gautier, Clement A ^a   Kitada, Tohru ^a   Shen, Jie ^a  

^a HARVARD MEDICAL SCHOOL   (United States)

Author keywords

Genetic Parkinson's disease; Knockout; Neurodegeneration; PARK6; Parkinsonism

Indexed keywords

MITOCHONDRIAL PROTEIN; PROTEIN PINK1;

ARTICLE; BRAIN CORTEX; CITRIC ACID CYCLE; CONTROLLED STUDY; GENE DELETION; GENE LOSS; GENE MUTATION; MITOCHONDRION; MOUSE; NONHUMAN; OXIDATIVE STRESS; PARKINSON DISEASE; PRIORITY JOURNAL;

ANIMALS; CEREBRAL CORTEX; CITRIC ACID CYCLE; CORPUS STRIATUM; GENE DELETION; GERM-LINE MUTATION; HEAT-SHOCK RESPONSE; HYDROGEN PEROXIDE; MICE; MICE, KNOCKOUT; MITOCHONDRIA; MITOCHONDRIAL DISEASES; MITOCHONDRIAL PROTEINS; OXIDATIVE STRESS; OXYGEN CONSUMPTION; PARKINSON DISEASE; PROTEIN KINASES; TIME FACTORS;

MAMMALIA; MUS;

EID: 49649097747     PISSN: 00278424     EISSN: 10916490     Source Type: Journal    
DOI: 10.1073/pnas.0802076105     Document Type: Article

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