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Journal of Biological Chemistry

Volumn 275, Issue 52, 2000, Pages 40916-40924

Ras inactivation of the retinoblastoma pathway by distinct mechanisms in NIH 3T3 fibroblast and RIE-1 epithelial cells

(3) Pruitt, Kevin a Pestell, Richard G b Der, Channing J a,c

a UNIVERSITY OF NORTH CAROLINA SCHOOL OF MEDICINE (United States)

b ALBERT EINSTEIN CANCER CENTER (United States)

c UNIVERSITY OF NORTH CAROLINA (United States)

Author keywords

[No Author keywords available]

Indexed keywords

CYCLIN D1; PHOSPHATIDYLINOSITOL 3 KINASE; PROTEIN P21; PROTEIN P27; RAF PROTEIN; RAS PROTEIN; RETINOBLASTOMA PROTEIN; TRANSCRIPTION FACTOR AP 1;

ANIMAL CELL; ARTICLE; CELL CYCLE; CELL STIMULATION; CELL TRANSFORMATION; CONTROLLED STUDY; DEREGULATION; DOWN REGULATION; FIBROBLAST; GENE ACTIVATION; INTESTINE EPITHELIUM CELL; MOUSE; NONHUMAN; ONCOGENE RAS; PRIORITY JOURNAL; PROTEIN EXPRESSION; PROTEIN PHOSPHORYLATION; STEADY STATE;

1-PHOSPHATIDYLINOSITOL 3-KINASE; 3T3 CELLS; ANIMALS; CELL CYCLE; CELL TRANSFORMATION, NEOPLASTIC; CYCLIN D1; CYCLIN-DEPENDENT KINASE INHIBITOR P21; CYCLINS; GENES, RAS; INTESTINAL MUCOSA; MICE; MICROFILAMENT PROTEINS; MUSCLE PROTEINS; PHOSPHORYLATION; PROTO-ONCOGENE PROTEINS C-RAF; RETINOBLASTOMA PROTEIN;

ANIMALIA;

EID: 0034731364 PISSN: 00219258 EISSN: None Source Type: Journal
DOI: 10.1074/jbc.M006682200 Document Type: Article

Times cited : (26)

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