Binds to Rb. Mutants in this region are defective in induction of focus formation. Nuclear transport defective mutants of large T have been analysed, when such a mutation is transfected into primary cells it does not transform suggesting a nuclear function. However, transformation of NIH 3T3 cells is as efficient as the wild type gene. Here it is assumed to be functioning in the cytoplasm.
Mechanism of action is probably via an interaction with tumour suppressor genes.
Rb-p105 is a phosphorylated nuclear protein which modulates transcription. Rb gene identified in individuals who develop retinoblastoma early in life. T antigen association with these 2 proteins is postulated to overcome the inhibition of cell growth. Human serotypes transform rat cells and some cause tumours in hamsters but natural infections have not been shown to cause transformation. The E1A protein is nuclear and phosphorylated at multiple serine residues, acidic and proline rich.