ArticleThe Journal of general virology2012
Activation of the STAT6 transcription factor in Jurkat T-cells by the herpesvirus saimiri Tip protein.
Article in The Journal of general virology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 14 citations in OpenAlex.
- Characterization of a Cytokine-Independent STAT5 Activator.Biomedicines · 2026Article
- An engineered viral protein activates STAT5 to prevent T cell suppression.Science immunology · 2025Article
- Human germline heterozygous gain-of-function STAT6 variants cause severe allergic disease.The Journal of experimental medicine · 2023Article
- The Dynamic Interface of Viruses with STATs.Journal of virology · 2020Review
- STAT6 degradation and ubiquitylated TRIML2 are essential for activation of human oncogenic herpesvirus.PLoS pathogens · 2018Article
- Nuclear Localization and Cleavage of STAT6 Is Induced by Kaposi's Sarcoma-Associated Herpesvirus for Viral Latency.PLoS pathogens · 2017Article
- The Modulation of Apoptotic Pathways by Gammaherpesviruses.Frontiers in microbiology · 2016Review
- Constitutive Activation of Interleukin-13/STAT6 Contributes to Kaposi's Sarcoma-Associated Herpesvirus-Related Primary Effusion Lymphoma Cell Proliferation and Survival.Journal of virology · 2015Article
- Viral proteins and Src family kinases: Mechanisms of pathogenicity from a "liaison dangereuse".World journal of virology · 2013Review
- A molecular model for the differential activation of STAT3 and STAT6 by the herpesviral oncoprotein tip.PloS one · 2012Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
Abstract
Herpesvirus saimiri (HVS), a T-lymphotropic monkey herpesvirus, induces fulminant T-cell lymphoma in non-natural primate hosts. In addition, it can immortalize human T-cells in vitro. HVS tyrosine kinase-interacting protein (Tip) is an essential viral gene required for T-cell transformation both in vitro and in vivo. In this study, we found that Tip interacts with the STAT6 transcription factor and induces phosphorylation of STAT6 in T-cells. The interaction with STAT6 requires the Tyr(127) residue and Lck-binding domain of Tip, which are indispensable for interleukin (IL)-2-independent T-cell transformation by HVS. It was also demonstrated that Tip induces nuclear translocation of STAT6, as well as activation of STAT6-dependent transcription in Jurkat T-cells. Interestingly, the phosphorylated STAT6 mainly colocalized with vesicles containing Tip within T-cells, but was barely detectable in the nucleus. However, nuclear translocation of phospho-STAT6 and transcriptional activation of STAT6 by IL-4 stimulation were not affected significantly in T-cells expressing Tip. Collectively, these findings suggest that the constitutive activation of STAT6 by Tip in T-cells may contribute to IL-2-independent T-cell transformation by HVS.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.