Revelation of p53-independent function of MTA1 in DNA damage response via modulation of the p21WAF1-proliferating cell nuclear antigen pathway

Journal of Biological Chemistry

Volumn 285, Issue 13, 2010, Pages 10044-10052

  Li, Da Qiang ^a   Pakala, Suresh B ^a   Reddy, Sirigiri Divijendra Natha ^a   Ohshiro, Kazufumi ^a   Peng, Shao Hua ^a,b   Lian, Yi ^a   Fu, Sidney W ^a   Kumar, Rakesh ^a  

^a GEORGE WASHINGTON UNIVERSITY MEDICAL CENTER   (United States)

^b UNIVERSITY OF TEXAS   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

COREPRESSORS; DAMAGE-RESPONSE PATHWAYS; DEACETYLASE; DNA DAMAGE RESPONSE; DNA DAMAGES; DNA DOUBLE STRAND BREAKS; DNA REPAIR; DOWN-REGULATION; HISTONE DEACETYLASES; INDEPENDENT FUNCTIONS; NUCLEAR ACCUMULATION; NUCLEOSOME REMODELING; PROLIFERATING CELL NUCLEAR ANTIGENS; PROMOTER ACTIVITIES; UNDERLYING MECHANISM;

ANTIGENS; DNA SEQUENCES; GENES; IONIZING RADIATION; PROTEINS; RADIATION SHIELDING; RADIOACTIVITY;

DNA;

CYCLIN DEPENDENT KINASE INHIBITOR 1; CYCLINE; HISTONE DEACETYLASE 2; METASTASIS ASSOCIATED PROTEIN 1; PROTEIN P53; UNCLASSIFIED DRUG; CELL NUCLEUS ANTIGEN; CYCLIN DEPENDENT KINASE INHIBITOR 1A; HISTONE DEACETYLASE; MTA1 PROTEIN, HUMAN; MTA1 PROTEIN, MOUSE; REPRESSOR PROTEIN; TRANSCRIPTION FACTOR;

ANIMAL CELL; ARTICLE; CONTROLLED STUDY; DNA DAMAGE; DOUBLE STRANDED DNA BREAK; DOWN REGULATION; GENE FUNCTION; HUMAN; HUMAN CELL; IONIZING RADIATION; MOUSE; NONHUMAN; NULL CELL; PRIORITY JOURNAL; PROMOTER REGION; PROTEIN BINDING; PROTEIN DEPLETION; TRANSCRIPTION REGULATION; ANIMAL; CELL NUCLEUS; CELL PROLIFERATION; DNA MICROARRAY; METABOLISM; MOUSE MUTANT; TUMOR CELL LINE;

ANIMALS; ANTIGENS, NUCLEAR; CELL LINE, TUMOR; CELL NUCLEUS; CELL PROLIFERATION; CYCLIN-DEPENDENT KINASE INHIBITOR P21; HISTONE DEACETYLASES; HUMANS; MICE; MICE, KNOCKOUT; OLIGONUCLEOTIDE ARRAY SEQUENCE ANALYSIS; PROLIFERATING CELL NUCLEAR ANTIGEN; PROMOTER REGIONS, GENETIC; REPRESSOR PROTEINS; TRANSCRIPTION FACTORS; TUMOR SUPPRESSOR PROTEIN P53;

EID: 77951219163     PISSN: 00219258     EISSN: 1083351X     Source Type: Journal    
DOI: 10.1074/jbc.M109.079095     Document Type: Article

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