Ability of a T-antigen transport-defective mutant of simian virus 40 to immortalize primary cells and to complement polyomavirus middle T in tumorigenesis.
AUTOR(ES)
Vass-Marengo, J
RESUMO
The oncogenic potential of polyomavirus in newborn rats could not be expressed by a genome encoding only the middle T antigen but required the presence of one of the other two viral early genes, small T or large T. The tumorigenicity defect could also be complemented by other viral or cellular genes that are known to be implicated in immortalization and establishment functions. The simian virus 40(cT)-3 mutant (R. E. Lanford and J. S. Butel, Cell 37:801-813, 1984), which fails to localize to the nucleus, has the capacity to complement polyomavirus middle T in tumorigenesis and to immortalize primary rat embryo fibroblasts when it was cotransfected in the presence of pSV2-neo. Our data suggested that under the conditions of DNA-mediated tumor induction and cotransfection with a dominant selection marker, the cellular alterations achieved by nonnuclear oncogenes such as polyomavirus small T and simian virus 40(cT)-3 were sufficient to complement polyomavirus middle T in transformation and tumorigenesis.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=253229Documentos Relacionados
- Differential ability of a T-antigen transport-defective mutant of simian virus 40 to transform primary and established rodent cells.
- Functional interaction of nuclear transport-defective simian virus 40 large T antigen with chromatin and nuclear matrix.
- Polyomavirus middle T-antigen NPTY mutants.
- Dimerization of simian virus 40 T-antigen hexamers activates T-antigen DNA helicase activity.
- Simian virus 40 mutant with transposed T-antigen and VP1 genes.