Interactions of SV40 large T-antigen and other viral proteins with retinoblstoma tumour suppressor

다국어 초록 (Multilingual Abstract)

The simian virus 40 large T antigen, the human papilloma virus E7 and the adenoviruse E1A are potent oncoproteins that can induce several types of tumours. One of the major functions of these oncoproteins is to interact with retinoblastoma tumor suppressor(Rb), a master switch of mammalian cell cycle, and to inactivate its function. Rb promotes cell cycle arrest by recruiting and regulating the proteins involved in transcription. The binding of viral oncoproteins to Rb disrupts the Rb-E2F complex, a central component in Rb mediated cell cycle network. The crystal structures of Rb pocket - viral oncoproeins complexes propose that the viral proteins recognizes the highly conserved region in the Rb pocket through their common motif, LxCxE, and through other unique regions within each viral protein. While the mechanism of Rb inactivation by viral proteins is not fully understood, we will present the atomic level information on the interactions of Rb pocket - viral protein complexes and discuss the insight how these proteins dissociate the E2F from Rb and how they deregulate the cell cycle.