ArticleJHEP reports : innovation in hepatology2025
NTCP ubiquitination enables HBV infection.
Article in JHEP reports : innovation in hepatology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- SCARF2 Mediates Intracellular Trafficking and Nucleocapsid Release of Hepatitis B Virus Within Hepatocytes.Journal of clinical and translational hepatology · 2026Article
- Post-Translational Modifications of NTCP: A Regulatory Nexus for Bile Acid Transport and HBV Entry.Biomedicines · 2026Review
- Serum PreS1 antigen combined with vascular endothelial growth factor can identify low-level hepatitis B virus DNA replication in patients with hepatitis B e antigen-negative chronic infection.American journal of translational research · 2026Article
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background & Aims: The sodium taurocholate cotransporting polypeptide (NTCP), the main hepatic uptake transporter of bile salts, is the docking receptor required for the HBV/HDV entry. However, the mechanism of NTCP-dependent internalization of HBV/HDV into hepatocytes is unclear. Thus, we investigated the contribution of post-translational modification of NTCP to transporter endocytosis and HBV infection. Methods: NTCP ubiquitination was determined by immunoprecipitation of wild-type NTCP (NTCP Results: NTCP was found to be ubiquitinated. Compared with NTCP Conclusions: K340 is essential for NTCP ubiquitination. Inhibiting ubiquitination impaired NTCP endocytosis and reduced HBV infection, confirming that NTCP-mediated endocytosis is critical for HBV hepatic entry. Impact and implications: This study contributes to elucidating the process of how HBV enters hepatocytes, which is largely elusive. NTCP was found not only to be required for the binding of HBV to hepatocytes, but also to have a crucial role in hepatic internalization of HBV. In addition, a K at position 340 was identified as the main ubiquitination target of NTCP; ubiquitination-mediated endocytosis of NTCP at this position is likely to be the mechanism regulating HBV internalization. Thus, interfering with NTCP ubiquitination could provide a novel means to reduce HBV infection.
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Registered trials
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