Akt Activation Protects Hippocampal Neurons from Apoptosis by Inhibiting Transcriptional Activity of p53

Journal of Biological Chemistry

Volumn 276, Issue 7, 2001, Pages 5256-5264

  Yamaguchi, Atsushi ^a,d   Tamatani, Michio ^a,d   Matsuzaki, Hideo ^a,d   Namikawa, Kazuhiko ^b   Kiyama, Hiroshi ^b,d   Vitek, Michael P ^c   Mitsuda, Noriaki ^a,d   Tohyama, Masaya ^a,d  

^a OSAKA UNIVERSITY GRADUATE SCHOOL OF MEDICINE   (Japan)

^b ASAHIKAWA MEDICAL COLLEGE   (Japan)

^c DUKE UNIVERSITY MEDICAL CENTER   (United States)

^d JAPAN SCIENCE AND TECHNOLOGY AGENCY   (Japan)

Author keywords

[No Author keywords available]

Indexed keywords

CELLS; GENES; HORMONES; NITROGEN COMPOUNDS; TOXICITY;

APOPTOSIS; HIPPOCAMPAL NEURONS; NUCLEAR TRANSLOCATION;

ENZYMES;

CASPASE; CASPASE 3; NITRIC OXIDE; PHOSPHATIDYLINOSITOL 3 KINASE INHIBITOR; PROTEIN KINASE B; PROTEIN P53; PROTEIN SERINE THREONINE KINASE; SOMATOMEDIN C; WORTMANNIN; CASP3 PROTEIN, MOUSE; DNA; ONCOPROTEIN; TRANSCRIPTION FACTOR;

ADENOVIRUS; ANIMAL CELL; APOPTOSIS; ARTICLE; BAX GENE; BRAIN CELL; CELL NUCLEUS; CELL PROTECTION; CYTOTOXICITY; EMBRYO; ENZYME ACTIVATION; GENE; GENE ACTIVATION; GENE EXPRESSION SYSTEM; GENE OVEREXPRESSION; GENETIC TRANSCRIPTION; HIPPOCAMPUS; HYPOXIA; INTRACELLULAR TRANSPORT; MOUSE; NERVE CELL NECROSIS; NEWBORN; NONHUMAN; PRIORITY JOURNAL; PROTEIN EXPRESSION; PROTEIN TRANSPORT; RAT; VIRUS RECOMBINANT; ACTIVE TRANSPORT; ANIMAL; C57BL MOUSE; CBA MOUSE; CELL CULTURE; CELL HYPOXIA; CYTOLOGY; DRUG EFFECT; ENZYMOLOGY; METABOLISM; NERVE CELL; PHYSIOLOGY; TRANSACTIVATION;

ADENOVIRIDAE; ANIMALIA;

ACTIVE TRANSPORT, CELL NUCLEUS; ANIMALS; APOPTOSIS; CASPASE 3; CASPASES; CELL HYPOXIA; CELL NUCLEUS; CELLS, CULTURED; DNA; ENZYME ACTIVATION; HIPPOCAMPUS; INSULIN-LIKE GROWTH FACTOR I; MICE; MICE, INBRED C57BL; MICE, INBRED CBA; NEURONS; NITRIC OXIDE; PROTEIN-SERINE-THREONINE KINASES; PROTO-ONCOGENE PROTEINS; PROTO-ONCOGENE PROTEINS C-AKT; TRANS-ACTIVATION (GENETICS); TRANSCRIPTION FACTORS; TUMOR SUPPRESSOR PROTEIN P53;

EID: 0035895964     PISSN: 00219258     EISSN: None     Source Type: Journal    
DOI: 10.1074/jbc.M008552200     Document Type: Article

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