Abstract
We have investigated the mechanisms by which the mos oncogene affects the phenotypes and genetic instability of transformed cells. Our laboratory discovered that the mos proto-oncogene, as a regulator of chromosome partitioning during meiosis, is required for the formation of an unfertilized egg (Sagata et al., Nature 355: 519–525, 1988; Yew et al., Current Opin. in Gen. & Dev. 3: 19–25, 1993). These observations led to our hypothesis that inappropriate expression of the Mos meiotic program in somatic cells results in cellular transformation by the mos oncogene.
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N. Sagatg, M. Oskarsson, T. Copeland, J. Brumbaugh, and G.F. Vande Woude, The c-mos proto-oncogene product functions during meiotic maturation in Xenopus oocytes, Nature 355: 519 (1988).
N. Yew, M. Strobel, and G.F. Vande Woude, Mos and the cell cycle: The molecular basis of the transformed phenotype, Current Opin. in Gen. & Dev. 3: 19 (1993).
J. Posada, N. Yew, N.G. Ahn, G.F. Vande Woude, and J.A. Cooper, Mos stimulates MAP kinase in Xenopus oocytes and activates a MAP kinase in vitro, Mol. Cell. Biol. 7: 2489 (1992).
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© 1994 Springer Science+Business Media New York
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Vande Woude, G.F., Choi, T., Zhou, R., Murakami, M., Matten, W., Fukasawa, K. (1994). Mos Proto-Oncogene and Cell Cycle Regulation. In: Hu, V.W. (eds) The Cell Cycle. GWUMC Department of Biochemistry Annual Spring Symposia. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-2421-2_29
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DOI: https://doi.org/10.1007/978-1-4615-2421-2_29
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