Stoichiometry of cellular and viral components in the polyomavirus middle-T antigen-tyrosine kinase complex

1990 ◽  
Vol 10 (10) ◽  
pp. 5569-5574
Author(s):  
S H Cheng ◽  
P C Espino ◽  
J Marshall ◽  
R Harvey ◽  
A E Smith
Keyword(s):  
Tyrosine Kinase ◽  
Tyrosine Kinases ◽  
Cellular Proliferation ◽  
T Antigen ◽  
Phosphatidylinositol Kinase ◽  
Polyomavirus Middle T Antigen ◽  
Viral Components ◽  
Middle T Antigen

Our results indicate that only one type of tyrosine kinase is present within each middle-T antigen-tyrosine kinase complex, suggesting that middle-T antigen forms separate complexes with different tyrosine kinases. Furthermore, we determined that there is only one molecule of middle-T antigen within any one of these complexes. We interpret this to mean that in any given cell, polyomavirus transformation involves, at least in part, the simultaneous deregulation of a number of separate pathways controlling cellular proliferation. Finally, we also demonstrate that the separate middle-T:pp60c-src and middle-T:pp59c-fyn complexes are each able to interact with the same cellular p81/85-kDa phosphoprotein, a possible component of the phosphatidylinositol kinase.

scholarly journals Stoichiometry of cellular and viral components in the polyomavirus middle-T antigen-tyrosine kinase complex.

1990 ◽  
Vol 10 (10) ◽  
pp. 5569-5574 ◽  
Author(s):  
S H Cheng ◽  
P C Espino ◽  
J Marshall ◽  
R Harvey ◽  
A E Smith
Keyword(s):  
Tyrosine Kinase ◽  
Tyrosine Kinases ◽  
Cellular Proliferation ◽  
T Antigen ◽  
Phosphatidylinositol Kinase ◽  
Polyomavirus Middle T Antigen ◽  
Viral Components ◽  
Middle T Antigen

Our results indicate that only one type of tyrosine kinase is present within each middle-T antigen-tyrosine kinase complex, suggesting that middle-T antigen forms separate complexes with different tyrosine kinases. Furthermore, we determined that there is only one molecule of middle-T antigen within any one of these complexes. We interpret this to mean that in any given cell, polyomavirus transformation involves, at least in part, the simultaneous deregulation of a number of separate pathways controlling cellular proliferation. Finally, we also demonstrate that the separate middle-T:pp60c-src and middle-T:pp59c-fyn complexes are each able to interact with the same cellular p81/85-kDa phosphoprotein, a possible component of the phosphatidylinositol kinase.

scholarly journals p56lck protein-tyrosine kinase is cytoskeletal and does not bind to polyomavirus middle T antigen.

1988 ◽  
Vol 62 (12) ◽  
pp. 4673-4679 ◽  
Author(s):  
R R Louie ◽  
C S King ◽  
A MacAuley ◽  
J D Marth ◽  
R M Perlmutter ◽  
...  
Keyword(s):  
Tyrosine Kinase ◽  
Protein Tyrosine Kinase ◽  
T Antigen ◽  
Protein Tyrosine ◽  
Polyomavirus Middle T Antigen ◽  
Middle T Antigen

Phosphatidylinositol metabolism in cells transformed by polyomavirus middle T antigen.

1990 ◽  
Vol 64 (8) ◽  
pp. 3895-3904 ◽  
Author(s):  
E T Ulug ◽  
P T Hawkins ◽  
M R Hanley ◽  
S A Courtneidge
Keyword(s):  
T Antigen ◽  
Phosphatidylinositol Metabolism ◽  
Polyomavirus Middle T Antigen ◽  
Middle T Antigen ◽  
In Cells

Recombinant retroviruses encoding simian virus 40 large T antigen and polyomavirus large and middle T antigens

1986 ◽  
Vol 6 (4) ◽  
pp. 1204-1217
Author(s):  
P S Jat ◽  
C L Cepko ◽  
R C Mulligan ◽  
P A Sharp
Keyword(s):  
Cell Lines ◽  
Simian Virus 40 ◽  
Simian Virus ◽  
T Antigen ◽  
Vector System ◽  
Large T Antigen ◽  
T Antigens ◽  
Sv40 Large T Antigen ◽  
Polyomavirus Middle T Antigen ◽  
Middle T Antigen

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.

Association of the polyomavirus middle-T antigen with c-yes protein

Nature ◽  
1987 ◽  
Vol 325 (6100) ◽  
pp. 171-173 ◽  
Author(s):  
Sally Kornbluth ◽  
Marius Sudol ◽  
Hidesaburo Hanafusa
Keyword(s):  
T Antigen ◽  
Polyomavirus Middle T Antigen ◽  
Middle T Antigen

scholarly journals Induction of mammary tumors by expression of polyomavirus middle T oncogene: a transgenic mouse model for metastatic disease.

1992 ◽  
Vol 12 (3) ◽  
pp. 954-961 ◽  
Author(s):  
C T Guy ◽  
R D Cardiff ◽  
W J Muller
Keyword(s):  
Transgenic Mice ◽  
Transcriptional Control ◽  
Mammary Epithelium ◽  
Metastatic Potential ◽  
T Antigen ◽  
Specific Expression ◽  
Mouse Mammary Tumor ◽  
Tumor Virus ◽  
Polyomavirus Middle T Antigen ◽  
Middle T Antigen

The effect of mammary gland-specific expression of the polyomavirus middle T antigen was examined by establishing lines of transgenic mice that carry the middle T oncogene under the transcriptional control of the mouse mammary tumor virus promoter/enhancer. By contrast to most transgenic strains carrying activated oncogenes, expression of polyomavirus middle T antigen resulted in the widespread transformation of the mammary epithelium and the rapid production of multifocal mammary adenocarcinomas. Interestingly, the majority of the tumor-bearing transgenic mice developed secondary metastatic tumors in the lung. Taken together, these results suggest that middle T antigen acts as a potent oncogene in the mammary epithelium and that cells that express it possess an enhanced metastatic potential.

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