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.
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Acknowledgements
We thank Dr S Goff for critically reading this manuscript and members of the Calame and Goff laboratories for helpful discussions. We would like to thank the following colleagues for their generous gifts of murine cDNAs: Dr David Cobrinik for cyclin E, Dr Berthold Henglein for cyclin A, and Dr Lars Thelander for ribonucleotide reductase. We would also like to thank Drs Jill Slansky and Peggy Farnham for the DHFR wild type and mutant promoter plasmids.
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Coutts, M., Zou, X. & Calame, K. v-Abl utilizes multiple mechanisms to drive G1/S progression in fibroblasts. Oncogene 19, 801–809 (2000). https://doi.org/10.1038/sj.onc.1203398
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DOI: https://doi.org/10.1038/sj.onc.1203398
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