Cross-reaction of BK virus large T antigen with monoclonal antibodies directed against SV40 large T antigen

Virology ◽  
1984 ◽  
Vol 138 (2) ◽  
pp. 379-385 ◽  
Author(s):  
Robert S. Mann ◽  
Robert B. Carroll
1998 ◽  
Vol 18 (3) ◽  
pp. 1746-1756 ◽  
Author(s):  
Kimya F. Harris ◽  
Joan B. Christensen ◽  
Eric H. Radany ◽  
Michael J. Imperiale

ABSTRACT E2F activity is regulated in part by the retinoblastoma family of tumor suppressor proteins. Viral oncoproteins, such as simian virus 40 (SV40) large-T antigen (TAg), adenovirus E1A, and human papillomavirus E7, can disrupt the regulation of cellular proliferation by binding to pRb family members and dissociating E2F-pRb family protein complexes. BK virus (BKV), which infects a large percentage of the human population and has been associated with a variety of human tumors, encodes a TAg homologous to SV40 TAg. It has been shown that BKV TAg, when expressed at low levels, does not detectably bind to pRb family members, yet it induces a serum-independent phenotype and causes a decrease in the overall levels of pRb family proteins. The experiments presented in this report show that, despite the lack of TAg-pRb interactions, BKV TAg can induce transcriptionally active E2F and that this induction does in fact require an intact pRb-binding domain as well as an intact J domain. In addition, E2F-pRb family member complexes can be detected in both BKV and SV40 TAg-expressing cells. These results suggest the presence of alternate cellular mechanisms for the release of E2F in addition to the well-established model for TAg-pRb interactions. These results also emphasize a role for BKV TAg in the deregulation of cellular proliferation, which may ultimately contribute to neoplasia.


1999 ◽  
Vol 44 (10) ◽  
pp. 823-834 ◽  
Author(s):  
M.H. Parkar ◽  
L. Kuru ◽  
M. O’Hare ◽  
H.N. Newman ◽  
F. Hughes ◽  
...  

Cell ◽  
1987 ◽  
Vol 48 (2) ◽  
pp. 321-330 ◽  
Author(s):  
Ilan Bikel ◽  
Ximena Montano ◽  
Mounzer E. Agha ◽  
Myles Brown ◽  
Melissa McCormack ◽  
...  

1986 ◽  
Vol 6 (4) ◽  
pp. 1204-1217
Author(s):  
P S Jat ◽  
C L Cepko ◽  
R C Mulligan ◽  
P A Sharp

We used a murine retrovirus shuttle vector system to construct recombinants capable of constitutively expressing the simian virus 40 (SV40) large T antigen and the polyomavirus large and middle T antigens as well as resistance to G418. Subsequently, these recombinants were used to generate cell lines that produced defective helper-free retroviruses carrying each of the viral oncogenes. These recombinant retroviruses were used to analyze the role of the viral genes in transformation of rat F111 cells. Expression of the polyomavirus middle T antigen alone resulted in cell lines that were highly tumorigenic, whereas expression of the polyomavirus large T resulted in cell lines that were highly tumorigenic, whereas expression of the polyomavirus large T resulted in cell lines that were unaltered by the criteria of morphology, anchorage-independent growth, and tumorigenicity. More surprisingly, SV40 large T-expressing cell lines were not tumorigenic despite the fact that they contained elevated levels of cellular p53 and had a high plating efficiency in soft agar. These results suggest that the SV40 large T antigen is not an acute transforming gene like the polyomavirus middle T antigen but is similar to the establishment genes such as myc and adenovirus EIa.


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