ArticleThe Journal of biological chemistry2017
Host transcription factor Speckled 110 kDa (Sp110), a nuclear body protein, is hijacked by hepatitis B virus protein X for viral persistence.
Article in The Journal of biological chemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed.
- The dynamic and heterogeneous composition of biomolecular condensates and its functional relevance.Nature reviews. Molecular cell biology · 2026Review
- An SP110-SP100 axis is a critical regulator of promyelocytic leukaemia body dynamics and mitotic fidelity.Nature cell biology · 2026Article
- Innate immune recognition in hepatitis B virus infection.Virulence · 2025Review
- Small molecule inhibition of SUMOylation increases expression from AAV vectors both during and after initial transduction in mice.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Differential impact of hepatitis delta virus replication and expression of viral antigens on the cellular kinome profile.Cell communication and signaling : CCS · 2025Article
- TRIM28 functions as SUMO ligase to SUMOylate TRAF6 and regulate NF-κB activation in HBV-replicating cells.Hepatology international · 2025Article
- SP110 Could be Used as a Potential Predictive and Therapeutic Biomarker for Oral Cancer.Molecular biotechnology · 2025Article
- Decoding microbial carcinogenic strategies: ubiquitination and SUMO modification.Frontiers in microbiology · 2025Review
- Comparative proteomic analysis of PK-15 cells infected with wild-type strain and its EP0 gene-deleted mutant strain of pseudorabies virus.Journal of veterinary science · 2024Article
- Abnormal protein SUMOylation in liver disease: novel target for therapy.Journal of molecular medicine (Berlin, Germany) · 2024Review
- SUMO Modification of Hepatitis B Virus Core Mediates Nuclear Entry, Promyelocytic Leukemia Nuclear Body Association, and Efficient Formation of Covalently Closed Circular DNA.Microbiology spectrum · 2023Article
- The interactions between PML nuclear bodies and small and medium size DNA viruses.Virology journal · 2023Review
- Review
- Regulation of Pattern-Recognition Receptor Signaling by HBX During Hepatitis B Virus Infection.Frontiers in immunology · 2022Review
- The emerging role of DEAD/H-box helicases in hepatitis B virus infection.Frontiers in cellular and infection microbiology · 2022Review
- Viruses, SUMO, and immunity: the interplay between viruses and the host SUMOylation system.Journal of neurovirology · 2021Review
- Silencing hepatitis B virus covalently closed circular DNA: The potential of an epigenetic therapy approach.World journal of gastroenterology · 2021Review
- SUMO and SUMOylation Pathway at the Forefront of Host Immune Response.Frontiers in cell and developmental biology · 2021Review
- Single Hepatocyte Hepatitis B Virus Transcriptional Landscape in HIV Coinfection.The Journal of infectious diseases · 2020Article
- Article
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5 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Promyelocytic leukemia nuclear bodies (PML-NB) are sub-nuclear organelles that are the hub of numerous proteins. DNA/RNA viruses often hijack the cellular factors resident in PML-NBs to promote their proliferation in host cells. Hepatitis B virus (HBV), belonging to Hepadnaviridae family, remains undetected in early infection as it does not induce the innate immune response and is known to be the cause of several hepatic diseases leading to cirrhosis and hepatocellular carcinoma. The association of PML-NB proteins and HBV is being addressed in a number of recent studies. Here, we report that the PML-NB protein Speckled 110 kDa (Sp110) is SUMO1-modified and undergoes a deSUMOylation-driven release from the PML-NB in the presence of HBV. Intriguingly, Sp110 knockdown significantly reduced viral DNA load in the culture supernatant by activation of the type I interferon-response pathway. Furthermore, we found that Sp110 differentially regulates several direct target genes of hepatitis B virus protein X (HBx), a viral co-factor. Subsequently, we identified Sp110 as a novel interactor of HBx and found this association to be essential for the exit of Sp110 from the PML-NB during HBV infection and HBx recruitment on the promoter of these genes. HBx, in turn, modulates the recruitment of its associated transcription cofactors p300/HDAC1 to these co-regulated genes, thereby altering the host gene expression program in favor of viral persistence. Thus, we report a mechanism by which HBV can evade host immune response by hijacking the PML-NB protein Sp110, and therefore, we propose it to be a novel target for antiviral therapy.
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