Dysregulation of the MEK/ERK/MNK1 signalling cascade by middle T antigen of the trichoydsplasia spinulosa polyomavirus

2017 ◽  
Vol 31 (8) ◽  
pp. 1338-1341 ◽  
Author(s):  
J.H. Wu ◽  
D. Narayanan ◽  
R.A. Simonette ◽  
P.L. Rady ◽  
S.K. Tyring
Keyword(s):  
T Antigen ◽  
Middle T Antigen ◽  
Signalling Cascade

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

scholarly journals Role of the Three Polyoma Virus Early Proteins in Tumorigenesis

1983 ◽  
Vol 3 (8) ◽  
pp. 1451-1459 ◽  
Author(s):  
Claude Asselin ◽  
Celine Gelinas ◽  
Marcel Bastin
Keyword(s):  
Cultured Cells ◽  
Virus Genome ◽  
T Antigen ◽  
Polyoma Virus ◽  
Transformed Cells ◽  
Newborn Rats ◽  
Wild Type ◽  
Complementary Function ◽  
Small T Antigen ◽  
Middle T Antigen

A modified polyoma virus genome which can encode the middle T protein but not the large or small T proteins transforms rat cells in culture with an efficiency about 20% that of the wild-type genome. Although middle T-transformed cells grow as tumors when transplanted into nude mice or syngeneic rats, the middle T gene alone is totally inactive when used in a more stringent and rigorous assay for tumorigenicity such as the injection of DNA into newborn rats. Thus, functions other than those expressed by middle T antigen are required for the elaboration of all the properties associated with tumorigenesis. To assess whether a complementary function could be exerted by the large or the small T antigen, we constructed plasmids containing two modified early regions which independently encoded middle T and one of the two other proteins. Both recombinants were tumorigenic in newborn rats. Cell lines derived by transfer of these plasmids under no special selective conditions did not acquire the property of growth in low-serum medium but exhibited the same tumorigenic properties as wild-type polyoma DNA-transformed cells. Furthermore, a recombinant which encoded the middle and small T antigens, but not the large T antigen, was tumorigenic in newborn rats. Although the small T antigen provides a complementary function for tumorigenicity, it cannot complement the middle T antigen for an efficient induction of transformation of cultured cells. This suggests that the complementary function exerted by the small T antigen is different from that of the N-terminal fragment of the large T protein.

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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