ArticleJournal of virology1997
Transformation and tumorigenic properties of a mutant polyomavirus containing a middle T antigen defective in Shc binding.
Article in Journal of virology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 18 citations in OpenAlex.
- A Transformation-Defective Polyomavirus Middle T Antigen with a Novel Defect in PI3 Kinase Signaling.Journal of virology · 2017Article
- Lessons in signaling and tumorigenesis from polyomavirus middle T antigen.Microbiology and molecular biology reviews : MMBR · 2009Review
- Lessons from polyoma middle T antigen on signaling and transformation: A DNA tumor virus contribution to the war on cancer.Virology · 2009Review
- Polyomavirus middle T antigen induces the transcription of osteopontin, a gene important for the migration of transformed cells.Journal of virology · 2008Article
- The p110alpha isoform of phosphatidylinositol 3-kinase is essential for polyomavirus middle T antigen-mediated transformation.Journal of virology · 2007Article
- Induction of polyomavirus-specific CD8(+) T lymphocytes by distinct dendritic cell subpopulations.Journal of virology · 2001Article
- Polyomavirus-infected dendritic cells induce antiviral CD8(+) T lymphocytes.Journal of virology · 2000Article
- Retinoic acid inhibits transformation by preventing phosphatidylinositol 3-kinase dependent activation of the c-fos promoter.Oncogene · 1999Article
- Signaling from polyomavirus middle T and small T defines different roles for protein phosphatase 2A.Molecular and cellular biology · 1998Article
- Requirement for both Shc and phosphatidylinositol 3' kinase signaling pathways in polyomavirus middle T-mediated mammary tumorigenesis.Molecular and cellular biology · 1998Article
- Serine 257 phosphorylation regulates association of polyomavirus middle T antigen with 14-3-3 proteins.Journal of virology · 1998Article
- Tumor induction by a transformation-defective polyoma virus mutant blocked in signaling through Shc.Proceedings of the National Academy of Sciences of the United States of America · 1997Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Polyomavirus middle T antigen is phosphorylated on several tyrosine residues which act as binding sites for cellular proteins, including phosphatidylinositol 3-kinase, Shc, and phospholipase C-gamma. In this report we describe the transforming properties and tumor-inducing ability of a polyomavirus that contains a single-site mutation in middle T antigen which changes a tyrosine residue at amino acid position 250 to serine. This mutation disrupts the association of middle T with the transforming protein Shc. The mutant virus is weakly transforming, inducing foci which are smaller and of different morphology than those of the wild type. Although the virus induced tumors in close to 100% of inoculated mice, the spectrum of tumors and their morphology were altered compared to those of wild-type virus. The mutant virus induced a reduced frequency of kidney and thymic tumors. Both the mammary gland and the thymic tumors that were induced were histologically distinct from those induced by wild-type polyomavirus. These results demonstrate that the signal transduction pathway that is deregulated by the middle T-Shc association is important for full transformation of cells in culture and for tumor induction in some target tissues in the mouse-polyomavirus system.
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