The codon 72 polymorphism-specific effects of human p53 are absent in mouse cells: Implications on generation of mouse models

Oncogene

Volumn 26, Issue 21, 2007, Pages 2964-2974

  Phang, B H ^a   Sabapathy, K ^a,b  

^a DIVISION OF MEDICAL ONCOLOGY   (Singapore)

^b NATIONAL UNIVERSITY OF SINGAPORE   (Singapore)

Author keywords

Codon 72 polymorphism; CRM1; Growth inhibition; MDM2; Mouse cells; p53

Indexed keywords

CHIMERIC PROTEIN; EXPORTIN 1; PROTEIN MDM2; PROTEIN P53;

ANIMAL CELL; ARTICLE; CELL CYCLE ARREST; CELL CYCLE G0 PHASE; CELL CYCLE G1 PHASE; CELL GROWTH; CODON; CONTROLLED STUDY; EXON; EXPERIMENTAL MODEL; GENE FUNCTION; GENETIC POLYMORPHISM; HUMAN; HUMAN CELL; MOUSE; NONHUMAN; PRIORITY JOURNAL; PROTEIN FUNCTION; REGULATORY MECHANISM; SPECIES DIFFERENCE; TRANSCRIPTION INITIATION; TUMOR SUPPRESSOR GENE;

ANIMALS; CELL LINE, TUMOR; CODON; DISEASE MODELS, ANIMAL; GROWTH INHIBITORS; HUMANS; MICE; ONCOGENE PROTEINS, FUSION; POLYMORPHISM, GENETIC; PROTEIN BINDING; PROTO-ONCOGENE PROTEINS C-MDM2; TUMOR SUPPRESSOR PROTEIN P53;

MUS;

EID: 34248391761     PISSN: 09509232     EISSN: 14765594     Source Type: Journal    
DOI: 10.1038/sj.onc.1210112     Document Type: Article

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