Viral oncoprotein binding to pRB, p107, p130, and p300.
The purpose of this review is to bring attention to some additional work in the tumor virus/tumor suppressor field which may have been overshadowed by reports describing adenovirus, SV40, and HPV oncoprotein binding to pRB and p53. The data reviewed herein provide further support for the model that a common mechanism by which DNA tumor viruses transform cells involves inactivation of cellular proteins which function as negative regulators of cell growth.
Ludlow
J W
JW
Department of Biochemistry, School of Medicine and Dentistry, Rochester, NY 14642, USA.
Skuse
G R
GR
D000818:Animals; D000952:Antigens, Polyomavirus Transforming / Q000378:metabolism*; D004263:DNA Tumor Viruses / Q000378:metabolism*; D006801:Humans; D009687:Nuclear Proteins / Q000378:metabolism; D009856:Oncogene Proteins, Viral / Q000378:metabolism*; D010750:Phosphoproteins; D011506:Proteins / Q000378:metabolism; D016160:Retinoblastoma Protein / Q000378:metabolism*; D050720:Retinoblastoma-Like Protein p107; D050717:Retinoblastoma-Like Protein p130; D015534:Trans-Activators; D014157:Transcription Factors / Q000378:metabolism
D000952:Antigens, Polyomavirus Transforming; D009687:Nuclear Proteins; D009856:Oncogene Proteins, Viral; D010750:Phosphoproteins; D011506:Proteins; C493844:RBL1 protein, human; C493837:RBL2 protein, human; D016160:Retinoblastoma Protein; D050720:Retinoblastoma-Like Protein p107; D050717:Retinoblastoma-Like Protein p130; D015534:Trans-Activators; D014157:Transcription Factors