ArticleMolecular cell2012
Viral E3 ubiquitin ligase-mediated degradation of a cellular E3: viral mimicry of a cellular phosphorylation mark targets the RNF8 FHA domain.
Article in Molecular cell, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
What it found
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Who cites it
53 citing papers in PubMed, 81 citations in OpenAlex.
- Riddle syndrome with RNF168 mutation in first Asian family cluster exhibiting pulmonary fibrosis and achalasia.Journal of human genetics · 2026Article
- SUMOylation and ubiquitination reciprocally regulate SMCHD1 antiviral activity against herpes simplex virus 1.PLoS pathogens · 2026Article
- Post-translational modifications as a key mechanism for herpes simplex virus type I evasion of host innate immunity.Frontiers in microbiology · 2025Review
- Conserved linear motif within the immediate early protein ORF45 promotes its engagement with KSHV lytic cycle-promoting forkhead transcription factors, FOXK1 and FOXK2.Journal of virology · 2024Article
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- SARS-CoV-2 and the DNA damage response.The Journal of general virology · 2023Review
- How different viruses perturb host cellular machinery via short linear motifs.EXCLI journal · 2023Review
- A 77 Amino Acid Region in the N-Terminal Half of the HSV-1 E3 Ubiquitin Ligase ICP0 Contributes to Counteracting an Established Type 1 Interferon Response.Microbiology spectrum · 2022Article
- Interactome and Ubiquitinome Analyses Identify Functional Targets of Herpes Simplex Virus 1 Infected Cell Protein 0.Frontiers in microbiology · 2022Article
- Comparative proteomics identifies Schlafen 5 (SLFN5) as a herpes simplex virus restriction factor that suppresses viral transcription.Nature microbiology · 2021Article
- Evasion of Intracellular DNA Sensing by Human Herpesviruses.Frontiers in cellular and infection microbiology · 2021Review
- "Non-Essential" Proteins of HSV-1 with Essential Roles In Vivo: A Comprehensive Review.Viruses · 2020Review
- The Race between Host Antiviral Innate Immunity and the Immune Evasion Strategies of Herpes Simplex Virus 1.Microbiology and molecular biology reviews : MMBR · 2020Review
- The HSV-1 ubiquitin ligase ICP0: Modifying the cellular proteome to promote infection.Virus research · 2020Review
- Effect of SUMO-SIM Interaction on the ICP0-Mediated Degradation of PML Isoform II and Its Associated Proteins in Herpes Simplex Virus 1 Infection.Journal of virology · 2020Article
- Review
- Human papillomavirus E7 oncoprotein targets RNF168 to hijack the host DNA damage response.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Genome and Environmental Activity of aFrontiers in microbiology · 2019Article
- Host Intrinsic and Innate Intracellular Immunity During Herpes Simplex Virus Type 1 (HSV-1) Infection.Frontiers in microbiology · 2019Review
Corrections and comments
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Authors and funding
12 authors at 7 institutions in 2 countries.
Funding
Abstract
Viral hijacking of cellular processes relies on the ability to mimic the structure or function of cellular proteins. Many viruses encode ubiquitin ligases to facilitate infection, although the mechanisms by which they select their substrates are often unknown. The Herpes Simplex Virus type-1-encoded E3 ubiquitin ligase, ICP0, promotes infection through degradation of cellular proteins, including the DNA damage response E3 ligases RNF8 and RNF168. Here we describe a mechanism by which this viral E3 hijacks a cellular phosphorylation-based targeting strategy to degrade RNF8. By mimicking a cellular phosphosite, ICP0 binds RNF8 via the RNF8 forkhead associated (FHA) domain. Phosphorylation of ICP0 T67 by CK1 recruits RNF8 for degradation and thereby promotes viral transcription, replication, and progeny production. We demonstrate that this mechanism may constitute a broader viral strategy to target other cellular factors, highlighting the importance of this region of the ICP0 protein in countering intrinsic antiviral defenses.
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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.