ArticleThe Journal of biological chemistry2020
The machinery for endocytosis of epidermal growth factor receptor coordinates the transport of incoming hepatitis B virus to the endosomal network.
Article in The Journal of biological chemistry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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Who cites it
53 citing papers in PubMed, 54 citations in OpenAlex.
- Review
- Review
- Post-Translational Modifications of NTCP: A Regulatory Nexus for Bile Acid Transport and HBV Entry.Biomedicines · 2026Review
- Insight into the Biology of Hepatitis B Virus and Recent Therapeutic Approaches.Current microbiology · 2026Review
- Structural mapping of NTCP distinguishes its dual functionality as a hepatitis B virus receptor and bile acid transporter.PLoS pathogens · 2026Article
- Niemann-Pick type C1 protein regulates epidermal growth factor receptor stability in hepatic cells and facilitates the early steps of Hepatitis B virus infection.Frontiers in cellular and infection microbiology · 2026Article
- Netrin-1 inhibits the attachment and internalization of Hepatitis B virus for hepatocyte infection.PLoS pathogens · 2025Article
- NTCP ubiquitination enables HBV infection.JHEP reports : innovation in hepatology · 2025Article
- Hepatitis B and D virus entry.Nature reviews. Microbiology · 2025Review
- HBV cccDNA: The Molecular Reservoir of Hepatitis B Persistence and Challenges to Achieve Viral Eradication.Biomolecules · 2025Review
- Potential role of epidermal growth factor receptors (EGFR) signaling in the pathogenesis and management of hepatocellular carcinoma.BioImpacts : BI · 2025Review
- Manganese is a potent inducer of lysosomal activity that inhibits de novo HBV infection.PLoS pathogens · 2025Article
- Hepatitis B virus entry, assembly, and egress.Microbiology and molecular biology reviews : MMBR · 2024Review
- SARS-CoV-2 aberrantly elevates mitochondrial bioenergetics to induce robust virus propagation.Signal transduction and targeted therapy · 2024Article
- Viruses exploit growth factor mechanisms to achieve augmented pathogenicity and promote tumorigenesis.Archives of microbiology · 2024Review
- Dysfunction and regulatory interplay of T and B cells in chronic hepatitis B: immunotherapy and emerging antiviral strategies.Frontiers in cellular and infection microbiology · 2024Review
- Deciphering the phospho-signature induced by hepatitis B virus in primary human hepatocytes.Frontiers in microbiology · 2024Article
- Coordinated ASBT and EGFR Mechanisms for Optimized Liraglutide Nanoformulation Absorption in the GI Tract.International journal of nanomedicine · 2024Article
- The Culprit Behind HBV-Infected Hepatocytes: NTCP.Drug design, development and therapy · 2024Review
- Role of Virus-Induced EGFR Trafficking in Proviral Functions.Biomolecules · 2023Review
Corrections and comments
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Authors and funding
18 authors at 8 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sodium taurocholate cotransporting polypeptide (NTCP) is expressed at the surface of human hepatocytes and functions as an entry receptor of hepatitis B virus (HBV). Recently, we have reported that epidermal growth factor receptor (EGFR) is involved in NTCP-mediated viral internalization during the cell entry process. Here, we analyzed which function of EGFR is essential for mediating HBV internalization. In contrast to the reported crucial function of EGFR-downstream signaling for the entry of hepatitis C virus (HCV), blockade of EGFR-downstream signaling proteins, including mitogen-activated protein kinase (MAPK), phosphoinositide 3-kinase (PI3K), and signal transducer and activator of transcription (STAT), had no or only minor effects on HBV infection. Instead, deficiency of EGFR endocytosis resulting from either a deleterious mutation in EGFR or genetic knockdown of endocytosis adaptor molecules abrogated internalization of HBV via NTCP and prevented viral infection. EGFR activation triggered a time-dependent relocalization of HBV preS1 to the early and late endosomes and to lysosomes in concert with EGFR transport. Suppression of EGFR ubiquitination by site-directed mutagenesis or by knocking down two EGFR-sorting molecules, signal-transducing adaptor molecule (STAM) and lysosomal protein transmembrane 4β (LAPTM4B), suggested that EGFR transport to the late endosome is critical for efficient HBV infection. Cumulatively, these results support the idea that the EGFR endocytosis/sorting machinery drives the translocation of NTCP-bound HBV from the cell surface to the endosomal network, which eventually enables productive viral 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.