ArticleJournal of virology1997
Herpesvirus saimiri Tip-484 membrane protein markedly increases p56lck activity in T cells.
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 20 papers.
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Who cites it
20 citing papers in PubMed, 53 citations in OpenAlex.
- Modulating p56Lck in T-Cells by a Chimeric Peptide Comprising Two Functionally Different Motifs of Tip from Herpesvirus saimiri.Journal of immunology research · 2015Article
- Actin-dependent activation of serum response factor in T cells by the viral oncoprotein tip.Cell communication and signaling : CCS · 2012Article
- Viral modulation of T-cell receptor signaling.Journal of virology · 2008Review
- Functional characterization and conformational analysis of the Herpesvirus saimiri Tip-C484 protein.Journal of molecular biology · 2007Article
- Growth transformation of human T cells by herpesvirus saimiri requires multiple Tip-Lck interaction motifs.Journal of virology · 2006Article
- HIV-1 Nef selectively activates Src family kinases Hck, Lyn, and c-Src through direct SH3 domain interaction.The Journal of biological chemistry · 2006Article
- T-cell growth transformation by herpesvirus saimiri is independent of STAT3 activation.Journal of virology · 2005Article
- Distinct roles of cellular Lck and p80 proteins in herpesvirus saimiri Tip function on lipid rafts.Journal of virology · 2003Article
- Herpesvirus saimiri.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2001Review
- Review
- Primary structure of the Herpesvirus ateles genome.Journal of virology · 2000Article
- Herpesvirus ateles gene product Tio interacts with nonreceptor protein tyrosine kinases.Journal of virology · 1999Article
- Altered expression of tyrosine kinases of the Src and Syk families in human T-cell leukemia virus type 1-infected T-cell lines.Journal of virology · 1999Article
- The Lck binding domain of herpesvirus saimiri tip-484 constitutively activates Lck and STAT3 in T cells.Journal of virology · 1999Article
- Identification of kaposin (open reading frame K12) as a human herpesvirus 8 (Kaposi's sarcoma-associated herpesvirus) transforming gene.Journal of virology · 1998Article
- Mutation of the Lck-binding motif of Tip enhances lymphoid cell activation by herpesvirus saimiri.Journal of virology · 1998Article
- STP and Tip are essential for herpesvirus saimiri oncogenicity.Journal of virology · 1998Article
- The superantigen-homologous viral immediate-early gene ie14/vsag in herpesvirus saimiri-transformed human T cells.Journal of virology · 1997Article
- Enhanced downregulation of Lck-mediated signal transduction by a Y114 mutation of herpesvirus Saimiri tip.Journal of virology · 1997Article
- Activation of STAT transcription factors by herpesvirus Saimiri Tip-484 requires p56lck.Journal of virology · 1997Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Herpesvirus saimiri (HVS) is a T-cell-specific transforming and oncogenic virus. A protein encoded by HVS known as Tip-484 (for tyrosine kinase interacting protein from HVS strain 484) is required for this transformation. Tip-484 binds specifically to the nonreceptor protein tyrosine kinase p56lck. By transfecting Tip-484 into T cells, we now show that this interaction leads to a several hundred-fold increase in the kinase activity of p56lck. Tip-484 is part of a protein complex which is dependent on the presence of p56lck and is phosphorylated. We also show that two of the complexed proteins represent two phosphorylated forms of Tip-484. Furthermore, the p56lck kinase activity in HVS-infected human peripheral blood T lymphocytes was at least ninefold higher than that in noninfected control cells and significantly decreased in cells infected with a Tip-484 deletion mutant virus. Finally, we report that Tip-484 is required for oncogenesis in rabbits by the survival of rabbits inoculated with Tip-484 deletion mutant HVS. The data demonstrate dramatic stimulation of the signaling pathway of p56lck. This effect can contribute to the molecular mechanisms that lead to sustained autocrine secretion of growth factors, permanent T-cell growth, and ultimately lymphocytic tumor formation.
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