Disrupted mitochondrial electron transport function increases expression of anti-apoptotic bcl-2 and bcl-X(L) proteins in SH-SYS5Y neuroblastoma and in parkinson disease cybrid cells through oxidative stress

Journal of Neuroscience Research

Volumn 61, Issue 6, 2000, Pages 693-700

  Veech, George A ^a   Dennis, Jameel ^a   Keeney, Paula M ^a   Fall, Christopher P ^a   Swerdlow, Russell H ^a   Davis Parker Jr , W ^a   Bennett Jr , James P ^a  

^a UNIVERSITY OF VIRGINIA HEALTH SYSTEM   (United States)

Author keywords

bcl 2; bcl X(L); Cybrids; Methylpyridinium; Oxidative stress; Parkinson disease

Indexed keywords

PROTEIN BCL 2; PROTEIN BCL X; REACTIVE OXYGEN METABOLITE;

ARTICLE; CELL CULTURE; CELL SURVIVAL; CONTROLLED STUDY; HUMAN; HUMAN CELL; NERVE CELL NECROSIS; NERVE DEGENERATION; NEUROBLASTOMA; OXIDATIVE STRESS; PARKINSON DISEASE; PATHOPHYSIOLOGY; PRIORITY JOURNAL; PROTEIN EXPRESSION; RESPIRATORY CHAIN; TRANSCRIPTION REGULATION;

1-METHYL-4-PHENYLPYRIDINIUM; APOPTOSIS; BCL-X PROTEIN; DNA, MITOCHONDRIAL; ELECTRON TRANSPORT; GENE EXPRESSION REGULATION; HERBICIDES; HUMANS; HYBRID CELLS; MICROSCOPY, CONFOCAL; MITOCHONDRIA; NEUROBLASTOMA; NEURONS; OXIDATIVE STRESS; PARKINSON DISEASE; PROTO-ONCOGENE PROTEINS C-BCL-2; RNA, MESSENGER; TUMOR CELLS, CULTURED;

EID: 0034666630     PISSN: 03604012     EISSN: None     Source Type: Journal    
DOI: 10.1002/1097-4547(20000915)61:6<693::AID-JNR13>3.0.CO;2-4     Document Type: Article

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