INTERACTIONS BETWEEN SV40 LARGE-TUMOR ANTIGEN AND THE GROWTH SUPPRESSOR PROTEIN-PRB AND PROTEIN-P53

The oncogenic property of simian virus 40 depends in large part on the function of the virus-coded T-antigen. Although the precise mechanism of how T functions during neoplastic transformation is not clear, som e answers to this question may lie in our understanding the nature of the proteins found to complex with T. The cellular protein p53 is perh aps the most extensively studied protein in this regard. Recently, p53 was defined as a growth suppressor protein. At about this same time, T was found to complex with another cell growth suppressor protein, th e product of the retinoblastoma susceptibility gene. It has since beco me apparent that complex formation between these proteins affects thei r individual growth-modulating activities. Quite often this alteration of activity correlates with an uncontrolled proliferative state of th e cell. Thus, transformation by SV40 is thought to involve complex for mation between the viral T oncoprotein and cellular growth suppressor proteins. This complex formation is believed to result in nullificatio n of the growth suppressor protein properties, thus increasing the pro pensity of the cell toward uncontrolled growth, the hallmark of neopla stic transformation.