ArticleVirology2017
The Itch ubiquitin ligase is required for KSHV RTA induced vFLIP degradation.
Article in Virology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
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Who cites it
13 citing papers in PubMed, 19 citations in OpenAlex.
- Analysis of the ubiquitin-modified proteome identifies novel host factors in Kaposi's sarcoma herpesvirus lytic reactivation.Journal of virology · 2025Article
- RUNX3 inhibits KSHV lytic replication by binding to the viral genome and repressing transcription.Journal of virology · 2024Article
- Kaposi's sarcoma herpesvirus viral FLICE inhibitory protein modulates A20 deubiquitinase activity.Access microbiology · 2024Article
- E3 Ubiquitin Ligases in Gammaherpesviruses and HIV: A Review of Virus Adaptation and Exploitation.Viruses · 2023Review
- Liver X Receptor-Inducible Host E3 Ligase IDOL Targets a Human Cytomegalovirus Reactivation Determinant.Journal of virology · 2023Article
- Review
- KSHV RTA antagonizes SMC5/6 complex-induced viral chromatin compaction by hijacking the ubiquitin-proteasome system.PLoS pathogens · 2022Article
- KSHV RTA Induces Degradation of the Host Transcription Repressor ID2 To Promote the Viral Lytic Cycle.Journal of virology · 2022Article
- ITCH as a potential therapeutic target in human cancers.Seminars in cancer biology · 2020Review
- Modulation of virus-induced NF-κB signaling by NEMO coiled coil mimics.Nature communications · 2020Article
- The interplay between EBV and KSHV viral products and NF-κB pathway in oncogenesis.Infectious agents and cancer · 2020Review
- CADM1 is essential for KSHV-encoded vGPCR-and vFLIP-mediated chronic NF-κB activation.PLoS pathogens · 2018Article
- Molecular Biology of KSHV in Relation to HIV/AIDS-Associated Oncogenesis.Cancer treatment and researchArticle
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Expression of Kaposi's sarcoma herpesvirus vFLIP, a potent activator of NFkB signaling, promotes latency. Inhibition of NFkB signaling promotes lytic reactivation. We previously reported that lytic inducer, RTA, inhibits vFLIP induced NFkB signaling by inducing the degradation of vFLIP via the proteasome. Here we report that the cellular ubiquitin ligase, Itch, is required for RTA induced degradation of vFLIP. Expression of either Itch targeting shRNA or a dominant negative mutant of the ubiquitin ligase both increased the stability of vFLIP in the presence of RTA. Itch potently ubiquitinated vFLIP in vivo and in vitro. We provide evidence for interaction between RTA, vFLIP and Itch and we identified an RTA resistant mutant of vFLIP that is unable to interact with Itch. These observations contribute to our understanding of how RTA counteracts the activities of vFLIP.
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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.