ArticleJournal of virology1998
Mutation of the Lck-binding motif of Tip enhances lymphoid cell activation by herpesvirus saimiri.
Article in Journal of virology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 30 citations in OpenAlex.
- Characterization of a Cytokine-Independent STAT5 Activator.Biomedicines · 2026Article
- Unraveling clonal CD8 T cell expansion and identification of essential factors in γ-herpesvirus-induced lymphomagenesis.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Review
- Modulating p56Lck in T-Cells by a Chimeric Peptide Comprising Two Functionally Different Motifs of Tip from Herpesvirus saimiri.Journal of immunology research · 2015Article
- Growth transformation of human T cells by herpesvirus saimiri requires multiple Tip-Lck interaction motifs.Journal of virology · 2006Article
- Downregulation of p56(lck) tyrosine kinase activity in T cells of squirrel monkeys (Saimiri sciureus) correlates with the nontransforming and apathogenic properties of herpesvirus saimiri in its natural host.Journal of virology · 2001Article
- Herpesvirus saimiri.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2001Review
- Evolutionary aspects of oncogenic herpesviruses.Molecular pathology : MP · 2000Review
- Signaling activities of gammaherpesvirus membrane proteins.Journal of virology · 2000Review
- Herpesvirus ateles gene product Tio interacts with nonreceptor protein tyrosine kinases.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
- A role for herpesvirus saimiri orf14 in transformation and persistent infection.Journal of virology · 1998Article
- Substitution of ras for the herpesvirus saimiri STP oncogene in lymphocyte transformation.Journal of virology · 1998Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
The proline-rich SH3-binding (SH3B) motif of the tyrosine kinase-interacting protein (Tip) of herpesvirus saimiri (HVS) is required for binding to the cellular Src family kinase Lck. We constructed a mutant form of HVS in which prolines in the SH3B motif of Tip were altered to alanines. This mutant form of Tip was incapable of binding to Lck. The mutant virus, HVS/Tip mSH3B, retained its ability to immortalize common marmoset lymphocytes in culture. In fact, common marmoset lymphocytes immortalized by the HVS/Tip mSH3B mutant displayed increased expression of HLA-DR lymphocyte activation marker, an altered pattern of tyrosine phosphorylation, increased expression of the tyrosine kinase Lyn, and a shift in electrophoretic mobility of Lck compared to cells immortalized by wild-type HVS. Experimental infection of common marmosets resulted in fulminant lymphoma with both HVS/Tip mSH3B and wild-type HVS. However, HVS/Tip mSH3B produced greater infiltration of affected organs by proliferating lymphoid cells compared to wild-type HVS. These results demonstrate that Tip binding to Lck is not necessary for transformation and that abrogation of Tip binding to Lck alters the characteristics of transformed cells and the severity of the pathologic lesions.
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