ArticleThe Journal of general virology2015
Hepatitis C virus NS5A protein blocks epidermal growth factor receptor degradation via a proline motif- dependent interaction.
Article in The Journal of general virology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
16 citing papers in PubMed, 29 citations in OpenAlex.
- Article
- Chinese herbal medicines: the modifier of hepatocellular carcinoma targeting Wnt/β-catenin signaling pathway.Frontiers in pharmacology · 2025Review
- Unmet Needs in the Post-Direct-Acting Antiviral Era: Hepatocarcinogenesis After Hepatitis C Virus Eradication.The Journal of infectious diseases · 2023Article
- Recent Updates on Viral Oncogenesis: Available Preventive and Therapeutic Entities.Molecular pharmaceutics · 2023Review
- Hepatitis C virus alters the morphology and function of peroxisomes.Frontiers in microbiology · 2023Article
- Signaling Induced by Chronic Viral Hepatitis: Dependence and Consequences.International journal of molecular sciences · 2022Review
- The Eukaryotic Linear Motif resource: 2022 release.Nucleic acids research · 2022Article
- Profibrotic Signaling and HCC Risk during Chronic Viral Hepatitis: Biomarker Development.Journal of clinical medicine · 2021Review
- Tracking Down the Epigenetic Footprint of HCV-Induced Hepatocarcinogenesis.Journal of clinical medicine · 2021Review
- Hepatocellular Carcinoma Mechanisms Associated with Chronic HCV Infection and the Impact of Direct-Acting Antiviral Treatment.Journal of hepatocellular carcinoma · 2020Review
- Wnt/β-Catenin Signaling in Liver Cancers.Cancers · 2019Review
- Oncogenic Signaling Induced by HCV Infection.Viruses · 2018Review
- Nonstructural Protein 5A Impairs DNA Damage Repair: Implications for Hepatitis C Virus-Mediated Hepatocarcinogenesis.Journal of virology · 2018Article
- Action and function of Wnt/β-catenin signaling in the progression from chronic hepatitis C to hepatocellular carcinoma.Journal of gastroenterology · 2017Review
- Large-Scale Screening of Preferred Interactions of Human Src Homology-3 (SH3) Domains Using Native Target Proteins as Affinity Ligands.Molecular & cellular proteomics : MCP · 2016Article
- EGFR Signaling in Liver Diseases.International journal of molecular sciences · 2015Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Hepatitis C virus (HCV) establishes a persistent infection that in many cases leads to cirrhosis and hepatocellular carcinoma. The non-structural 5A protein (NS5A) has been implicated in this process as it contains a C-terminal polyproline motif (termed P2) that binds to Src homology 3 (SH3) domains to regulate cellular signalling and trafficking pathways. We have shown previously that NS5A impaired epidermal growth factor (EGF) receptor (EGFR) endocytosis, thereby inhibiting EGF-stimulated EGFR degradation by a mechanism that remained unclear. As EGFR has been implicated in HCV cell entry and trafficking of the receptor involves several SH3-domain containing proteins, we investigated in more detail the mechanisms by which NS5A perturbs EGFR trafficking. We demonstrated that the P2 motif was required for the NS5A-mediated disruption to EGFR trafficking. We further demonstrated that the P2 motif was required for an interaction between NS5A and CMS, a homologue of CIN85 that has previously been implicated in EGFR endocytosis. We provided evidence that CMS was involved in the NS5A-mediated perturbation of EGFR trafficking. We also showed that NS5A effected a loss of EGFR ubiquitination in a P2-motif-dependent fashion. These data provide clues to the mechanism by which NS5A regulates the trafficking of a key cellular receptor and demonstrate for the first time the ability of NS5A to regulate host cell ubiquitination pathways.
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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.