The long term goal of this program is to understand the biochemical mechanisms which underlie neoplastic transformation by papovaviruses. In particular, the application describes experiments (by Drs. T. Roberts, A. Smith, D. Livingston, and B. Schaffhausen) designed to decipher the mode of action of three major species of papovaviral transforming proteins - SV40 large T, polyoma middle t, and polyoma large T. In particular, emphasis will be placed on how these proteins function as perturbants of the action of known cellular oncogene and anti-oncogene products and how the resulting perturbations are converted into growth altering signals. In addition, there will be a systematic genetic analysis (by Dr. R. Garcea in collaboration with Dr. T. Benjamin) of the receptor binding function of the major viral capsid protein of polyoma, VP1. Specific receptor binding, is essential to the progression of natural infection, to the development of virus-induced tumors, and, most likely, to the appearance of a mitogenic response to viral infection. Nevertheless, little is known of how the virus interacts with its receptor or how this structure functions, once activated.
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