Atm is dispensable for p53 apoptosis and tumor suppression triggered by cell cycle dysfunction

Molecular and Cellular Biology

Volumn 19, Issue 4, 1999, Pages 3095-3102

  Liao, Mai Jing ^a   Yin, Chaoying ^a   Barlow, Carrolee ^b   Wynshaw Boris, Anthony ^b   Van Dyke, Terry ^a,c  

^a UNIVERSITY OF NORTH CAROLINA SCHOOL OF MEDICINE   (United States)

^b NATIONAL HUMAN GENOME RESEARCH INSTITUTE   (United States)

^c UNIVERSITY OF NORTH CAROLINA   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

ATM PROTEIN; GENE PRODUCT; PROTEIN P53; UNCLASSIFIED DRUG;

ANIMAL TISSUE; APOPTOSIS; ARTICLE; ATAXIA TELANGIECTASIA; CANCER INHIBITION; CANCER SUSCEPTIBILITY; CELL CYCLE; CONTROLLED STUDY; DNA DAMAGE; MOUSE; NONHUMAN; ONCOGENE; PRIORITY JOURNAL; TRANSACTIVATION; TRANSGENIC MOUSE; TUMOR GROWTH; TUMOR SUPPRESSOR GENE;

ANIMALIA; ATAXIA; ATAXIA TELANGIECTASIA; MURINAE; MUS MUSCULUS; SIMIAE; SIMIAN VIRUS; SIMIAN VIRUS 40;

EID: 0032949352     PISSN: 02707306     EISSN: None     Source Type: Journal    
DOI: 10.1128/MCB.19.4.3095     Document Type: Article

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