ArticlePLoS pathogens2018
STAT6 degradation and ubiquitylated TRIML2 are essential for activation of human oncogenic herpesvirus.
Article in PLoS pathogens, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 17 citations in OpenAlex.
- Oncogenic viral infection triggers LAMP2A SUMOylation and chaperone-mediated autophagy to promote tumorigenesis.Nature microbiology · 2026Article
- Repression of EEF1D by KSHV RTA promotes viral lytic reactivation.Journal of virology · 2026Article
- The function of TRIML2 on the temozolomide resistance in glioblastoma.Annals of medicine and surgery (2012) · 2025Article
- Review
- Degradation of TRIM32 is induced by RTA for Kaposi's sarcoma-associated herpesvirus lytic replication.Journal of virology · 2024Article
- TRAF3/STAT6 axis regulates macrophage polarization and tumor progression.Cell death and differentiation · 2023Article
- Review
- Correction: STAT6 degradation and ubiquitylated TRIML2 are essential for activation of human oncogenic herpesvirus.PLoS pathogens · 2022Article
- RNA Microarray-Based Comparison of Innate Immune Phenotypes between Human THP-1 Macrophages Stimulated with Two BCG Strains.International journal of molecular sciences · 2022Article
- The regulation of KSHV lytic reactivation by viral and cellular factors.Current opinion in virology · 2022Review
- STAT6 contributes to renal fibrosis by modulating PPARα-mediated tubular fatty acid oxidation.Cell death & disease · 2022Article
- The Dynamic Interface of Viruses with STATs.Journal of virology · 2020Review
- STUB1 is targeted by the SUMO-interacting motif of EBNA1 to maintain Epstein-Barr Virus latency.PLoS pathogens · 2020Article
- Eutherian-Specific Gene TRIML2 Attenuates Inflammation in the Evolution of Placentation.Molecular biology and evolution · 2020Article
- Bixin Protects Against Kidney Interstitial Fibrosis Through Promoting STAT6 Degradation.Frontiers in cell and developmental biology · 2020Article
- KSHV: Immune Modulation and Immunotherapy.Frontiers in immunology · 2019Review
Corrections and comments
- Correction · 2022-06-01Error in Data · Error in Image ·
- Erratum issued
Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aberrations in STAT6-mediated signaling are linked to the development of multiple cancer types. Increasing evidence has shown that activation of human oncogenic herpesvirus lytic replication is crucial for viral tumorigenesis. However, the role of STAT6 in herpesvirus lytic replication remains elusive. Here, by using Kaposi's sarcoma-associated herpesvirus (KSHV) as a model, we revealed that RTA, the master regulator of lytic replication, interacts with STAT6 and promotes lysine 48 (K48) and K63-linked ubiquitylation of STAT6 for degradation via the proteasome and lysosome systems. Moreover, degradation of STAT6 is dramatically associated with the increased ubiquitylated form of tripartite motif family like 2 (TRIML2, a tumor suppressor) for prolonged cell survival and virion production, which is also commonly observed in lytic activation of Epstein-Barr virus, herpes simplex virus 1 and cytomegalovirus. These results suggest that degradation of STAT6 is important for the lytic activation of KSHV and as such, may be an attractive therapeutic target.
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