ArticleJournal of virology2018
The Human Papillomavirus E6 Oncoprotein Targets USP15 and TRIM25 To Suppress RIG-I-Mediated Innate Immune Signaling.
Article in Journal of virology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 99 papers.
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Who cites it
99 citing papers in PubMed, 138 citations in OpenAlex.
- Antiviral regulator TRIM25 as a prognostic marker of better survival in Merkel cell carcinoma: Association with MCPyV status.International journal of cancer · 2026Article
- Structural insights into ubiquitin recognition by USP15 revealed through a covalent activity-based probe.Communications biology · 2026Article
- Article
- Cervical human papillomavirus: the therapeutic target of botanical drugs.Frontiers in pharmacology · 2026Review
- Genome-wide association study identifies and validates genetic variation in the RIG-I/MAVS signaling pathway associated with HIV-related Kaposi sarcoma in children and adults.Frontiers in oncology · 2026Article
- Ubiquitination dynamics in human tumour viruses: Viral infection, oncogenesis and antiviral therapy.The FEBS journal · 2026Review
- HPV-driven inflammatory pathways in ovarian carcinogenesis: molecular mechanisms and emerging therapeutic interventions.Journal of ovarian research · 2025Review
- Human papillomavirus-related oropharyngeal squamous cell carcinoma exhibits enhanced radiosensitivity despite limited activation of cytosolic DNA sensing pathways and innate immune responses.Radiology and oncology · 2025Article
- PRRSV GP2a blocks the RLR signaling pathway by targeting RIG-I.Journal of virology · 2025Article
- Targeted degradation of the HPV oncoprotein E6 reduces tumor burden in cervical cancer.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Human Papillomavirus Integration Induces Oncogenic Host Gene Fusions in Oropharyngeal Cancers.Cancer discovery · 2025Article
- Genome Editing in Gynecological Oncology: The Emerging Role of CRISPR/Cas9 in Precision Cancer Therapy.Therapeutic innovation & regulatory science · 2025Review
- TRIM23 mediates cGAS-induced autophagy in anti-HSV defense.Nature communications · 2025Article
- Atypical MAPKs in cancer.The FEBS journal · 2025Review
- HPV16 E7 inhibits HBD2 expression by down-regulation of ASK1-p38 MAPK pathway in cervical cancer.Virology journal · 2025Article
- Virus-mediated immunosuppression in head and neck cancer.Oncogene · 2025Review
- Sexually transmitted human papillomavirus and related sequelae.Clinical microbiology reviews · 2025Review
- Dendritic cell-based immunotherapy for head and neck squamous cell carcinoma: advances and challenges.Frontiers in immunology · 2025Review
- Patterns of immune cell infiltration and oxidative stress in cervical cancer.Oncology reviews · 2025Review
- HPV and co-infections: impacts on semen inflammation, oxidative stress, and sperm quality.Frontiers in cellular and infection microbiology · 2025Article
39 more citing papers are in PubMed but not listed here.
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Authors and funding
10 authors at 5 institutions in 1 country.
Funding
Abstract
Retinoic acid-inducible gene I (RIG-I) is a key pattern recognition receptor that senses viral RNA and interacts with the mitochondrial adaptor MAVS, triggering a signaling cascade that results in the production of type I interferons (IFNs). This signaling axis is initiated by K63-linked ubiquitination of RIG-I mediated by the E3 ubiquitin ligase TRIM25, which promotes the interaction of RIG-I with MAVS. USP15 was recently identified as an upstream regulator of TRIM25, stabilizing the enzyme through removal of degradative K48-linked polyubiquitin, ultimately promoting RIG-I-dependent cytokine responses. Here, we show that the E6 oncoprotein of human papillomavirus type 16 (HPV16) as well as of other HPV types form a complex with TRIM25 and USP15 in human cells. In the presence of E6, the K48-linked ubiquitination of TRIM25 was markedly increased, and in line with this, TRIM25 degradation was enhanced. Our results further showed that E6 inhibited the TRIM25-mediated K63-linked ubiquitination of RIG-I and its CARD-dependent interaction with MAVS. HPV16 E6, but not E7, suppressed the RIG-I-mediated induction of IFN-β, chemokines, and IFN-stimulated genes (ISGs). Finally, CRISPR-Cas9 gene targeting in human keratinocytes showed that the TRIM25-RIG-I-MAVS triad is important for eliciting an antiviral immune response to HPV16 infection. Our study thus identifies a novel immune escape mechanism that is conserved among different HPV strains and further indicates that the RIG-I signaling pathway plays an important role in the innate immune response to HPV infection.
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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.