p19ARF is dispensable for oncogenic stress-induced p53-mediated apoptosis and tumor suppression in vivo

Molecular and Cellular Biology

Volumn 22, Issue 1, 2002, Pages 370-377

  Tolbert, D ^a   Lu, X ^a   Yin, C ^a   Tantama, M ^a   Van Dyke, T ^a  

^a UNIVERSITY OF NORTH CAROLINA   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

PROTEIN P19; PROTEIN P53; RNA;

ANIMAL MODEL; APOPTOSIS; ARTICLE; BRAIN TUMOR; CELL CYCLE; CELL SPECIFICITY; CELL TYPE; IN SITU HYBRIDIZATION; MOUSE; NONHUMAN; PRIORITY JOURNAL; TRANSGENIC MOUSE; TUMOR GROWTH; TUMOR SUPPRESSOR GENE;

ANIMALS; APOPTOSIS; CELL CYCLE PROTEINS; CELL DIVISION; CHOROID PLEXUS; CHOROID PLEXUS NEOPLASMS; CYCLIN-DEPENDENT KINASE INHIBITOR P16; CYCLIN-DEPENDENT KINASE INHIBITOR P21; CYCLINS; DISEASE MODELS, ANIMAL; DNA-BINDING PROTEINS; E2F TRANSCRIPTION FACTORS; E2F1 TRANSCRIPTION FACTOR; ENZYME INHIBITORS; EPITHELIAL CELLS; GENES, P16; HUMANS; IN SITU HYBRIDIZATION; IN SITU NICK-END LABELING; MICE; MICE, TRANSGENIC; NUCLEAR PROTEINS; ONCOGENE PROTEINS, VIRAL; PROTO-ONCOGENE PROTEINS; PROTO-ONCOGENE PROTEINS C-MDM2; SIGNAL TRANSDUCTION; TRANSCRIPTION FACTORS; TUMOR SUPPRESSOR PROTEIN P14ARF; TUMOR SUPPRESSOR PROTEIN P53; TUMOR SUPPRESSOR PROTEINS;

EID: 0036133649     PISSN: 02707306     EISSN: None     Source Type: Journal    
DOI: 10.1128/MCB.22.1.370-377.2002     Document Type: Article

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