Overexpression of mammalian Rad51 does not stimulate tumorigenesis while a dominant-negative Rad51 affects centrosome fragmentation, ploidy and stimulates tumorigenesis, in p53-defective CHO cells

Oncogene

Volumn 22, Issue 48, 2003, Pages 7587-7592

  Bertrand, Pascale ^a,b   Lambert, Sarah ^a,b   Joubert, Christophe ^b   Lopez, Bernard S ^a,b  

^a UMR CEA/CNRS 217   (France)

^b INSTITUT DE RADIOPROTECTION ET DE SÛRETÉ NUCLÉAIRE   (France)

Author keywords

Centrosome, aneuploidy; Homologous recombination; Rad51; Tumorigenesis

Indexed keywords

RAD51 PROTEIN; TUMOR SUPPRESSOR PROTEIN;

ANEUPLOIDY; ANIMAL CELL; ARTICLE; CARCINOGENESIS; CARCINOGENICITY; CELL STIMULATION; CENTROSOME; CHINESE HAMSTER; CHO CELL; CONTROLLED STUDY; FRAGMENTATION REACTION; GENE CONVERSION; GENE OVEREXPRESSION; GENE REPRESSION; NONHUMAN; NUDE MOUSE; PLOIDY; PRIORITY JOURNAL; PROTEIN INTERACTION; TUMOR SUPPRESSOR GENE;

ANEUPLOIDY; ANIMALS; CELL DIVISION; CENTROSOME; CHO CELLS; CRICETINAE; DNA FRAGMENTATION; DNA-BINDING PROTEINS; GENE CONVERSION; MICE; MICE, NUDE; MUTATION; NEOPLASM TRANSPLANTATION; NEOPLASMS; RAD51 RECOMBINASE; RECOMBINATION, GENETIC; TUMOR SUPPRESSOR PROTEIN P53;

ANIMALIA; CRICETINAE; CRICETULUS GRISEUS; MAMMALIA; MUS MUSCULUS;

EID: 0345304254     PISSN: 09509232     EISSN: None     Source Type: Journal    
DOI: 10.1038/sj.onc.1206998     Document Type: Article

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