BK virus large T antigen: interactions with the retinoblastoma family of tumor suppressor proteins and effects on cellular growth control

BK virus (BKV) is a polyomavirus which infects a large percentage of the human population. It is a potent transforming agent and is tumorigenic in rodents. BKV DNA has also been found in human brain, pancreatic islet, and urinary tract tumors, implicating this virus in neoplastic processes. BKV T an...

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Veröffentlicht in:Journal of virology Jg. 70; H. 4; S. 2378
Hauptverfasser: Harris, K F, Christensen, J B, Imperiale, M J
Format: Journal Article
Sprache:Englisch
Veröffentlicht: United States 01.04.1996
Schlagworte:
Animals
Antigens, Polyomavirus Transforming - metabolism
Antigens, Polyomavirus Transforming - physiology
BK Virus - immunology
BK Virus - physiology
Cell Division
Cell Line
Cell Transformation, Viral - physiology
Cercopithecus aethiops
Humans
Nuclear Proteins - metabolism
Phosphoproteins - metabolism
Protein Binding
Proteins
Retinoblastoma Protein - metabolism
Retinoblastoma-Like Protein p107
Retinoblastoma-Like Protein p130
Tumor Suppressor Protein p53 - metabolism
ISSN:0022-538X
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Zusammenfassung:BK virus (BKV) is a polyomavirus which infects a large percentage of the human population. It is a potent transforming agent and is tumorigenic in rodents. BKV DNA has also been found in human brain, pancreatic islet, and urinary tract tumors, implicating this virus in neoplastic processes. BKV T antigen (TAg) is highly homologous to simian virus 40 TAg, particularly in regions required for mitogenic stimulation and binding to tumor suppressor proteins, The experiments presented in this report show that BKV TAg can bind the tumor suppressor protein p53. BKV TAg also has the ability to bind to members of the retinoblastoma (pRb) family of tumor suppressor proteins both in vivo and in vitro. However, these interactions are detected only when large amounts of total protein are used, because the levels of BKV TAg normally produced from viral promoter-enhancer elements are too low to bind a significant amount of the pRb family proteins in the cell. The low levels of BKV TAg produced by the viral promoter elements are sufficient to affect the levels and the phosphorylation patterns of these proteins and to induce serum-independent growth in these cells. Additional events, however, are required for full transformation. These data further support the notion that BKV TAg can affect cellular growth control mechanisms and may in fact be involved in neoplastic processes.
Bibliographie:ObjectType-Article-1
SourceType-Scholarly Journals-1
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ISSN:0022-538X
DOI:10.1128/jvi.70.4.2378-2386.1996