MOZ increases p53 acetylation and premature senescence through its complex formation with PML

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

Volumn 110, Issue 10, 2013, Pages 3895-3900

  Rokudai, Susumu ^a   Laptenko, Oleg ^a   Arnal, Suzzette M ^a   Taya, Yoichi ^b   Kitabayashi, Issay ^c   Prives, Carol ^a  

^a Och Spine at New York Presbyterian Hospitals   (United States)

^b NATIONAL UNIVERSITY OF SINGAPORE   (Singapore)

^c NATIONAL CANCER CENTER RESEARCH INSTITUTE   (Japan)

Author keywords

DNA damage; Protein modification

Indexed keywords

ACYLTRANSFERASE; PROMYELOCYTIC LEUKEMIA PROTEIN; PROTEIN KINASE B; PROTEIN P53;

ACETYLATION; ARTICLE; CELL STRESS; HUMAN; HUMAN CELL; MOLECULAR RECOGNITION; MONOCYTIC LEUKEMIA ZINC FINGER; PRIORITY JOURNAL; PROMYELOCYTIC LEUKEMIA; PROTEIN EXPRESSION; PROTEIN PHOSPHORYLATION; PROTEIN PROTEIN INTERACTION; SENESCENCE; ZINC FINGER MOTIF;

ACETYLATION; ANIMALS; BASE SEQUENCE; CELL AGING; CELLS, CULTURED; CYCLIN-DEPENDENT KINASE INHIBITOR P21; GENE KNOCKOUT TECHNIQUES; HISTONE ACETYLTRANSFERASES; HUMANS; INTRANUCLEAR INCLUSION BODIES; LEUKEMIA, PROMYELOCYTIC, ACUTE; MICE; MODELS, BIOLOGICAL; MULTIPROTEIN COMPLEXES; P300-CBP TRANSCRIPTION FACTORS; PROTO-ONCOGENE PROTEINS C-AKT; RATS; RECOMBINANT PROTEINS; RNA, SMALL INTERFERING; TUMOR SUPPRESSOR PROTEIN P53;

EID: 84874594177     PISSN: 00278424     EISSN: 10916490     Source Type: Journal    
DOI: 10.1073/pnas.1300490110     Document Type: Article

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