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Title: v-Abl utilizes multiple mechanisms to drive G1/S progression in fibroblasts. Author: Coutts M, Zou X, Calame K. Journal: Oncogene; 2000 Feb 10; 19(6):801-9. PubMed ID: 10698498. Abstract: Transformation of 3T3 fibroblasts by the v-Abl tyrosine kinase replaces mitogenic and adhesion signals normally required for cell cycle progression. A 3T3 cell line conditionally transformed with v-Abl has been used to study v-Abl's effects on cell cycle in the context of either serum depletion or absence of adhesion signals. We show that E2F-dependent mRNAs, encoding proteins required for cell cycle progression, are induced by v-Abl. In addition, we identify two previously unknown targets of v-Abl signaling: (1) cyclin D1 and D2 mRNAs are induced upon v-Abl activation; and (2) the CDK inhibitor p27 is decreased upon v-Abl activation.[Abstract] [Full Text] [Related] [New Search]