ArticlePLoS pathogens2021
Multiple roles of PP2A binding motif in hepatitis B virus core linker and PP2A in regulating core phosphorylation state and viral replication.
Article in PLoS pathogens, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 50 citations in OpenAlex.
- Hepatitis B virus covalently closed circular DNA formation in murine hepatic cells uncovers a late entry block.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- CHB-Induced Immune Zonation Chaos Elicited LXRα-mediated Lipid Metabolism Disorders in Kupffer Cells to Induce Cancer Stem Cell Formation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Innate immune recognition and evasion strategies of hepatitis B virus: from DNA to RNA and viral proteins.Frontiers in immunology · 2026Review
- Hepatitis B Virus Nucleocapsid Assembly.Journal of molecular biology · 2025Review
- Serological and virological characterization of hepatitis B surface antigen-positive patients with or without Helicobacter pylori co-infection at the university of Gondar comprehensive specialized hospital, Northwest Ethiopia.BMC infectious diseases · 2025Article
- REGγ regulates antiviral response by activating TBK1-IFNβ signaling through degradation of PPP2CB.Cellular and molecular life sciences : CMLS · 2025Article
- New Advances in Small Molecules Targeted at Viral Capsid-Genome Binding.International journal of molecular sciences · 2025Review
- STK39 inhibits antiviral immune response by inhibiting DCAF1-mediated PP2A degradation.Acta pharmaceutica Sinica. B · 2025Article
- HBV polymerase recruits the phosphatase PP1 to dephosphorylate HBc-Ser170 to complete encapsidation.PLoS pathogens · 2025Article
- Article
- HBc: the multifunctional architect of HBV replication, immune evasion, and therapeutic innovation.Frontiers in immunology · 2025Review
- Clinical and biochemical characterization of hepatitis B surface antigen-positive patients with or withoutFrontiers in immunology · 2025Article
- Hepatitis B virus entry, assembly, and egress.Microbiology and molecular biology reviews : MMBR · 2024Review
- Epigenetic modification of hepatitis B virus infection and related hepatocellular carcinoma.Virulence · 2024Review
- Review
- Significance of hepatitis B virus capsid dephosphorylation via polymerase.Journal of biomedical science · 2024Article
- Emerging Roles of B56 Phosphorylation and Binding Motif in PP2A-B56 Holoenzyme Biological Function.International journal of molecular sciences · 2024Review
- Detection of Hepatitis B Virus Covalently Closed Circular DNA and Intermediates in Its Formation.Methods in molecular biology (Clifton, N.J.) · 2024Article
- A computational spatial whole-Cell model for hepatitis B viral infection and drug interactions.Scientific reports · 2023Article
- Hepatitis B core-related antigen: A novel and promising surrogate biomarker to guide anti-hepatitis B virus therapy.Clinical and molecular hepatology · 2023Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Hepatitis B virus (HBV) capsid or core protein (HBc) contains an N-terminal domain (NTD) and a C-terminal domain (CTD) connected by a short linker peptide. HBc plays a critical role in virtually every step of viral replication, which is further modulated by dynamic phosphorylation and dephosphorylation of its CTD. While several cellular kinases have been identified that mediate HBc CTD phosphorylation, there is little information on the cellular phosphatases that mediate CTD dephosphorylation. Herein, a consensus binding motif for the protein phosphatase 2A (PP2A) regulatory subunit B56 was recognized within the HBc linker peptide. Mutations within this motif designed to block or enhance B56 binding showed pleiotropic effects on CTD phosphorylation state as well as on viral RNA packaging, reverse transcription, and virion secretion. Furthermore, linker mutations affected the HBV nuclear episome (the covalently closed circular or CCC DNA) differentially during intracellular amplification vs. infection. The effects of linker mutations on CTD phosphorylation state varied with different phosphorylation sites and were only partially consistent with the linker motif serving to recruit PP2A-B56, specifically, to dephosphorylate CTD, suggesting that multiple phosphatases and/or kinases may be recruited to modulate CTD (de)phosphorylation. Furthermore, pharmacological inhibition of PP2A could decrease HBc CTD dephosphorylation and increase the nuclear HBV episome. These results thus strongly implicate the HBc linker in recruiting PP2A and other host factors to regulate multiple stages of HBV replication.
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