Deacetylation of p53 after nerve growth factor treatment in PC12 cells as a post-translational modification mechanism of neurotrophin-induced tumor suppressor activation

Oncogene

Volumn 23, Issue 49, 2004, Pages 8078-8087

  Vaghefi, Houman ^a   Neet, Kenneth E ^a  

^a ROSALIND FRANKLIN UNIVERSITY OF MEDICINE AND SCIENCE   (United States)

Author keywords

Acetylation; Apoptosis; Differentiation; Signal transduction

Indexed keywords

ANTIBODY; GROWTH FACTOR; HISTONE DEACETYLASE; LYSINE; MITOGEN ACTIVATED PROTEIN KINASE INHIBITOR; NERVE GROWTH FACTOR; NERVE GROWTH FACTOR RECEPTOR; NEUROTROPHIN; PROTEIN P53; TRANSCRIPTION FACTOR; TRICHOSTATIN A; TUMOR SUPPRESSOR PROTEIN; HYDROXAMIC ACID;

ACETYLATION; APOPTOSIS; ARTICLE; CANCER INHIBITION; CELL CYCLE; CELL CYCLE ARREST; CELL STRAIN; CONTROLLED STUDY; DEACETYLATION; DNA DAMAGE; DOSE TIME EFFECT RELATION; ENZYME ACTIVITY; FLUORESCENCE; GENE CONSTRUCT; HUMAN; HUMAN CELL; PRIORITY JOURNAL; PROTEIN PHOSPHORYLATION; PROTEIN PROCESSING; REPORTER GENE; TRANSACTIVATION; TRANSCRIPTION INITIATION; TUMOR SUPPRESSOR GENE; ANIMAL; DOSE RESPONSE; METABOLISM; PHYSIOLOGY; RAT; SIGNAL TRANSDUCTION;

ACETYLATION; ANIMALS; DOSE-RESPONSE RELATIONSHIP, DRUG; GENES, TUMOR SUPPRESSOR; HISTONE DEACETYLASES; HYDROXAMIC ACIDS; MAP KINASE SIGNALING SYSTEM; NERVE GROWTH FACTOR; PC12 CELLS; PROTEIN PROCESSING, POST-TRANSLATIONAL; RATS; TUMOR SUPPRESSOR PROTEIN P53;

EID: 7944236356     PISSN: 09509232     EISSN: None     Source Type: Journal    
DOI: 10.1038/sj.onc.1207953     Document Type: Article

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