Disruption of ATM in p53-null cells causes multiple functional abnormalities in cellular response to ionizing radiation

Oncogene

Volumn 18, Issue 50, 1999, Pages 7002-7009

  Takao, Noriaki ^a   Kato, Hideaki ^a   Mori, Ryoichi ^a   Morrison, Ciaran ^b   Sonada, Eiichiro ^b   Sun, Xiango ^a   Shimizu, Hiroko ^a   Yoshioka, Katsuji ^a   Takeda, Shunichi ^b   Yamamoto, Ken Ichi ^b  

^a KANAZAWA UNIVERSITY   (Japan)

^b KYOTO UNIVERSITY   (Japan)

Author keywords

ATM disruption; Cell cycle checkpoint; DNA repair; p53

Indexed keywords

DNA; PHOSPHATIDYLINOSITOL 3 KINASE; PROTEIN P53;

ANIMAL CELL; ARTICLE; ATAXIA TELANGIECTASIA; B LYMPHOCYTE; CELL CYCLE; CELL PROLIFERATION; CHROMOSOME ABERRATION; CONTROLLED STUDY; DNA INTEGRATION; DNA SYNTHESIS; GENE DISRUPTION; IONIZING RADIATION; MUTATION RATE; NONHUMAN; ONCOGENE; PRIORITY JOURNAL; RADIOSENSITIVITY;

ANIMALIA; ATAXIA; ATAXIA TELANGIECTASIA; GALLUS GALLUS;

EID: 0033604444     PISSN: 09509232     EISSN: None     Source Type: Journal    
DOI: 10.1038/sj.onc.1203172     Document Type: Article

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