Pronk. G. J. & Bos, J. L. The role of p21ras in receptor tyrosine kinase signalling. Biochim. Biophys.Acta1198, 131–147 (1994). PubMed Google Scholar
Marshall, C. J. Specificity of receptor tyrosine kinase signalling: transient versus sustained extracellular signal-regulated kinase activation. Cell8O, 179–185 (1995). Article Google Scholar
Dobrowolski, S., Harter, M. & Stacey, D. W. Cellular ras activity is required for passage through multiple points of the G0/G1 phase in Balb/c 3T3 cells. Mol. Cell. Biol.14, 5441–5449 (1994). ArticleCASPubMedPubMed Central Google Scholar
Feramisco, J. R., Gross, M., Kamata, T., Rosenberg, M. & Sweet, R. W. Microinjection of the oncogene form of the human H-ras (T-24) protein results in rapid proliferation of quiescent cells. Cell38, 109–117 (1984). ArticleCASPubMed Google Scholar
Stacey, D. W. & Kung, H. F. Transformation of NIH 3T3 cells by microinjection of Ha-ras protein. Nature310, 508–511 (1984). ArticleADSCASPubMed Google Scholar
Mulcahy, L. S., Smith, M. R. & Stacey, D. W. Requirement for ras proto-oncogene function during serum-stimulated growth of NIH 3T3 cells. Nature313, 241–243 (1985). ArticleADSCASPubMed Google Scholar
Lukas, J. et al. Retinoblastoma-protein-dependent cell-cycle inhibition by the tumour suppressor p16. Nature375, 503–506 (1995). ArticleADSCASPubMed Google Scholar
Koh, J., Enders, G. H., Dynlacht, B. D. & Harlow, E. Tumour-derived p16 alleles encoding proteins defective in cell-cycle inhibition. Nature375, 506–510 (1995). ArticleADSCASPubMed Google Scholar
Feig, L. A. & Cooper, G. M. Inhibition of NIH 3T3 cell proliferation by a mutant ras protein with preferential affinity for GDP. Mol. Cell. Biol.8, 3235–3243 (1988). ArticleCASPubMedPubMed Central Google Scholar
Cai, H., Szeberenyi, J. & Cooper, G. M. Effect of a dominant inhibitory Ha-ras mutation on mitogenic signal transduction. Mol. Cell. Biol.10, 5314–5323 (1990). ArticleCASPubMedPubMed Central Google Scholar
Medema, R. H., Herrera, R. E., Lam, F. & Weinberg, R. A. Growth suppression by p16ink4 requires functional retinoblastoma protein. Proc. Natl Acad. Sci. USA92, 6289–6293 (1995). ArticleADSCASPubMedPubMed Central Google Scholar
Guan, K.-L. et al. Growth suppression by p18, a p16INK4/MTSl- and p14INK4B/MTS2-related CDK6 inhibitor, correlates with wild-type pRb function. Genes Dev.8, 2939–2952 (1994). ArticleCASPubMed Google Scholar
Sherr, C. J. & Roberts, J. M. Inhibitors of mammalian Gl cyclin-dependent kinases. Genes Dev.9, 1149–1163 (1995). ArticleCASPubMed Google Scholar
Herrera, R. E. et al. Altered cell cycle kinetics, gene expression, and Gl restriction point regulation in Rb-deficient fibroblasts. Mol. Cell. Biol16, 2402–2407 (1996). ArticleCASPubMedPubMed Central Google Scholar
Lukas, J., Bartkova, J., Rohde, M., Strauss, M. & Bartek, J. Cyclin D1 is dispensable for G1 control in retinoblastoma gene-deficient cells independently of cdk4 activity. Mol. Cell. Biol.15, 2600–2611 (1995). ArticleCASPubMedPubMed Central Google Scholar
Lavoie, J. N., L'Allemain, G., Brunet, A., Muller, R. & Pouysségur, J. Cyclin D1 expression is regulated positively by the p42/p44MAPK and negatively by the p38/HOGMAPK pathway. J. Biol. Chem.271, 20608–20616 (1966). Article Google Scholar
Albanese, C. et al. Transforming p21ras mutants and c-Ets-2 activate the cyclin D1 promoter through distinguishable regions. J. Biol. Chem.270, 23589–23597 (1995). ArticleCASPubMed Google Scholar
Filmus, J. et al. Induction of cyclin D1 overexpression by activated ras. Oncogene9, 3627–3633 (1994). CASPubMed Google Scholar
Liu, J.-J. et al. Ras transformation results in an elevated level of cyclin D1 and acceleration of G1 progression in NIH 3T3 cells. Mol. Cell. Biol.15, 3654–3663 (1995). ArticleCASPubMedPubMed Central Google Scholar
Winston, J. T., Coats, S. R., Wang, Y.-Z. & Pledger, W. J. Regulation of the cell cycle machinery by oncogenic Ras. Oncogene12, 127–134 (1996). CASPubMed Google Scholar
Serrano, M., Gomez-Lohoz, E., DePinho, R. A., Beach, D. & Bar-Sagi, D. Inhibition of Ras-induced proliferation and transformation by p16INK4. Science267, 249–252 (1995). ArticleADSCASPubMed Google Scholar
Hatakeyama, M., Brill, J. A., Fink, G. R. & Weinberg, R. A. Collaboration of G1 cyclins in the functional inactivation of the retinoblastoma protein. Genes Dev.8, 1759–1771 (1994). ArticleCASPubMed Google Scholar
Zalvide, J. & DeCaprio, J. A. Role of pRb-related proteins in simian virus 40 large-T-antigen-mediated transformation. Mol. Cell. Biol15, 5800–5810 (1995). ArticleCASPubMedPubMed Central Google Scholar
Schneider, J. W., Gu, W., Zhu, L., Mahdavi, V. & Nadal-Ginard, B. Reversal of terminal differentiation mediated by p107 in Rb-/- muscle cells. Science264, 1467–1471 (1994). ArticleADSCASPubMed Google Scholar
Ewen, M. E. et al. Functional interactions of the retinoblastoma protein with mammalian D-type cyclins. Cell73, 487–497 (1993). ArticleCASPubMed Google Scholar
Serrano, M., Hannon, G. J. & Beach, D. A new regulatory motif in cell-cycle control causing specific inhibition of cyclin D/cdk4. Nature366, 704–707 (1993). ArticleADSCASPubMed Google Scholar
Ewen, M. E., Oliver, C. J., Sluss, H. K., Miller, S. J. & Peeper, D. S. p53-dependent repression of CDK4 translation in TGF-β-induced cell-cycle arrest. Genes Dev.9, 204–217 (1995). ArticleCASPubMed Google Scholar