CONTROL OF CELL-PROLIFERATION BY THE RETI NOBLASTOMA PROTEIN

Transformed cells proliferate abnormally, due to the unregulated activ ation of oncogenes and the inactivation of anti-oncogenes. The molecul ar mechanisms by which the product of the Rb antioncogene, the RE prot ein, regulates cell proliferation begin to be understood. Major target s of RE include proteins involved in cell cycle entry, like the E2F tr anscription factor, and effecters of terminal differentiation. The eff ect of RE is thus to block cells into the G1 phase of the cell cycle a nd to induce them to terminally differentiate. Recently, a new role ha s been shown for RE. RE is able to repress the activity of the RNA pol ymerases I and III, thereby modulating the protein biosynthesis capaci ties of the cell. RE appears thus to control directly the balance betw een DNA and protein synthesis during the cell cycle.