Long term lithium treatment suppresses p53 and Bax expression but increases Bcl-2 expression. A prominent role in neuroprotection against excitotoxicity

Journal of Biological Chemistry

Volumn 274, Issue 10, 1999, Pages 6039-6042

  Chen, Ren Wu ^a   Chuang, De Maw ^a  

^a NATIONAL INSTITUTE OF MENTAL HEALTH   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

CYTOCHROME C; GLUTAMIC ACID; LITHIUM CHLORIDE; PROTEIN BAX; PROTEIN BCL 2; PROTEIN P53;

ANIMAL CELL; APOPTOSIS; ARTICLE; BRAIN PROTECTION; CONTROLLED STUDY; DEPRESSION; DRUG MECHANISM; GRANULE CELL; LONG TERM CARE; NERVE DEGENERATION; NEUROTOXICITY; NONHUMAN; PRIORITY JOURNAL; PROTEIN EXPRESSION; RAT; TUMOR SUPPRESSOR GENE;

ANIMALS; BCL-2-ASSOCIATED X PROTEIN; CELLS, CULTURED; CEREBELLUM; DOWN-REGULATION; LITHIUM; NEURONS; PROTO-ONCOGENE PROTEINS; PROTO-ONCOGENE PROTEINS C-BCL-2; RATS; RATS, SPRAGUE-DAWLEY; RNA, MESSENGER; TUMOR SUPPRESSOR PROTEIN P53; UP-REGULATION;

EID: 0033525538     PISSN: 00219258     EISSN: None     Source Type: Journal    
DOI: 10.1074/jbc.274.10.6039     Document Type: Article

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