An HDAC1-binding domain within FATS bridges p21 turnover to radiation-induced tumorigenesis

Oncogene

Volumn 29, Issue 18, 2010, Pages 2659-2671

  Li, Z ^a   Zhang, Q ^b   Mao, J H ^c   Weise, A ^d   Mrasek, K ^d   Fan, X ^a   Zhang, X ^a   Liehr, T ^d   Lu, K H ^b   Balmain, A ^c   Cai, W W ^e  

^a BEIJING UNIVERSITY OF POSTS AND TELECOMMUNICATIONS   (China)

^b UNIVERSITY OF TEXAS   (United States)

^c UNIVERSITY OF CALIFORNIA   (United States)

^d Institute for Human Genetics and Anthropology   (Germany)

^e BAYLOR COLLEGE OF MEDICINE   (United States)

Author keywords

Acetylation; Carcinogenesis; P21; Radiation

Indexed keywords

AMIDE; HISTONE DEACETYLASE 1; PROTEIN P21;

ACETYLATION; AMINO TERMINAL SEQUENCE; ARTICLE; CONTROLLED STUDY; DNA DAMAGE; EXON; FRAGILE SITE ASSOCIATED TUMOR SUPPRESSOR GENE; GENE FUNCTION; GENETIC DAMAGE; GENETIC STABILITY; HETEROZYGOSITY LOSS; HUMAN; HUMAN CELL; PRIORITY JOURNAL; PROTEIN DOMAIN; RADIATION CARCINOGENESIS; THYMUS LYMPHOMA; TUMOR SUPPRESSOR GENE;

ACETYLATION; ANIMALS; BINDING SITES; CELL DIVISION; CHROMOSOME FRAGILE SITES; CYCLIN-DEPENDENT KINASE INHIBITOR P21; DNA DAMAGE; G2 PHASE; HISTONE DEACETYLASE 1; HUMANS; MICE; NEOPLASMS, RADIATION-INDUCED; NIH 3T3 CELLS; TUMOR SUPPRESSOR PROTEINS; UBIQUITINATION;

EID: 77952240146     PISSN: 09509232     EISSN: 14765594     Source Type: Journal    
DOI: 10.1038/onc.2010.19     Document Type: Article

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