ArticleJournal of virology2005
T-cell growth transformation by herpesvirus saimiri is independent of STAT3 activation.
Article in Journal of virology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 21 citations in OpenAlex.
- Network-based survival-associated module biomarker and its crosstalk with cell death genes in ovarian cancer.Scientific reports · 2015Article
- Actin-dependent activation of serum response factor in T cells by the viral oncoprotein tip.Cell communication and signaling : CCS · 2012Article
- Activation of the STAT6 transcription factor in Jurkat T-cells by the herpesvirus saimiri Tip protein.The Journal of general virology · 2012Article
- A molecular model for the differential activation of STAT3 and STAT6 by the herpesviral oncoprotein tip.PloS one · 2012Article
- Inhibition of retromer activity by herpesvirus saimiri tip leads to CD4 downregulation and efficient T cell transformation.Journal of virology · 2011Article
- Genome-wide histone acetylation profiling of Herpesvirus saimiri in human T cells upon induction with a histone deacetylase inhibitor.Journal of virology · 2011Article
- Role of amphipathic helix of a herpesviral protein in membrane deformation and T cell receptor downregulation.PLoS pathogens · 2008Article
- Persistent activation of STAT3 by latent Kaposi's sarcoma-associated herpesvirus infection of endothelial cells.Journal of virology · 2007Article
- Growth transformation of human T cells by herpesvirus saimiri requires multiple Tip-Lck interaction motifs.Journal of virology · 2006Article
- Association of herpesvirus saimiri tip with lipid raft is essential for downregulation of T-cell receptor and CD4 coreceptor.Journal of virology · 2006Article
- Tyrosine phosphorylation of the Tio oncoprotein is essential for transformation of primary human T cells.Journal of virology · 2005Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Herpesvirus saimiri (saimirine herpesvirus 2) (HVS), a T-lymphotropic tumor virus, induces lymphoproliferative disease in several species of New World primates. In addition, strains of HVS subgroup C are able to transform T cells of Old World primates, including humans, to permanently growing T-cell lines. In concert with the Stp oncoprotein, the tyrosine kinase-interacting protein (Tip) of HVS C488 is required for T-cell transformation in vitro and lymphoma induction in vivo. Tip was previously shown to interact with the protein tyrosine kinase Lck. Constitutive activation of signal transducers and activators of transcription (STATs) has been associated with oncogenesis and has also been detected in HVS-transformed T-cell lines. Furthermore, Tip contains a putative consensus YXPQ binding motif for the SH2 (src homology 2) domains of STAT1 and STAT3. Tip tyrosine phosphorylation at this site was required for binding of STATs and induction of STAT-dependent transcription. Here we sought to address the relevance of STAT activation for transformation of human T cells by introducing a tyrosine-to-phenylalanine mutation in the YXPQ motif of Tip of HVS C488. Unexpectedly, the recombinant virus was still able to transform human T lymphocytes, but it had lost its capability to activate STAT3 as well as STAT1. This demonstrates that growth transformation by HVS is independent of STAT3 activation.
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