Bcl-xL gain of function and p19ARF loss of function cooperate oncogenically with Myc in vivo by distinct mechanisms

Cancer Cell

Volumn 10, Issue 2, 2006, Pages 113-120

  Finch, Andrew ^a   Prescott, Julia ^b   Shchors, Ksenya ^a   Hunt, Abigail ^a   Soucek, Laura ^a   Dansen, Tobias B ^b   Swigart, Lamorna Brown ^a   Evan, Gerard I ^a  

^a UNIVERSITY OF CALIFORNIA   (United States)

^b NONE

Author keywords

CELLCYCLE

Indexed keywords

ARF PROTEIN; CYCLIN DEPENDENT KINASE INHIBITOR 1; MYC PROTEIN; PROTEIN BCL XL; PROTEIN P19; PROTEIN P53; BCL2L1 PROTEIN, MOUSE; CDKN1A PROTEIN, MOUSE; CDKN2A PROTEIN, MOUSE; CYCLIN DEPENDENT KINASE INHIBITOR 1A; PROTEIN BCL X; PROTEIN P14ARF; PROTEIN P16INK4A;

ANIMAL TISSUE; APOPTOSIS; ARTICLE; CARCINOGENESIS; CELL PROLIFERATION; CONTROLLED STUDY; GENE OVEREXPRESSION; KNOCKOUT MOUSE; MOUSE; NONHUMAN; ONCOGENE MYC; PANCREAS ISLET CELL; PRIORITY JOURNAL; PROTEIN FUNCTION; TRANSGENE; TRANSGENIC MOUSE; ANIMAL; CELL TRANSFORMATION; METABOLISM; PANCREAS ISLET BETA CELL; PATHOLOGY; PHYSIOLOGY;

ANIMALS; APOPTOSIS; BCL-X PROTEIN; CELL PROLIFERATION; CELL TRANSFORMATION, NEOPLASTIC; CYCLIN-DEPENDENT KINASE INHIBITOR P16; CYCLIN-DEPENDENT KINASE INHIBITOR P21; GENES, MYC; INSULIN-SECRETING CELLS; MICE; MICE, TRANSGENIC; TUMOR SUPPRESSOR PROTEIN P14ARF; TUMOR SUPPRESSOR PROTEIN P53;

EID: 33746803213     PISSN: 15356108     EISSN: None     Source Type: Journal    
DOI: 10.1016/j.ccr.2006.06.017     Document Type: Article

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