ArticleJournal of virology2016
Hepatocyte Factor JMJD5 Regulates Hepatitis B Virus Replication through Interaction with HBx.
Article in Journal of virology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 32 citations in OpenAlex.
- Alternative splicing regulatesiScience · 2026Article
- Potential for Core Fucose-Targeted Therapy Against HBV Infection of Human Normal Hepatocytes.Viruses · 2025Article
- Dual Role of Extracellular Vesicles as Orchestrators of Emerging and Reemerging Virus Infections.Cell biochemistry and biophysics · 2025Review
- Homeobox protein MSX-1 restricts hepatitis B virus by promoting ubiquitin-independent proteasomal degradation of HBx protein.PLoS pathogens · 2025Article
- Importin-7-dependent nuclear translocation of the Flavivirus core protein is required for infectious virus production.PLoS pathogens · 2024Article
- JMJD2D stabilises and cooperates with HBx protein to promote HBV transcription and replication.JHEP reports : innovation in hepatology · 2023Article
- 5-Substituted Pyridine-2,4-dicarboxylate Derivatives Have Potential for Selective Inhibition of Human Jumonji-C Domain-Containing Protein 5.Journal of medicinal chemistry · 2023Article
- The JMJD Family Histone Demethylases in Crosstalk Between Inflammation and Cancer.Frontiers in immunology · 2022Review
- Screening of the HBx transactivation domain interacting proteins and the function of interactor Pin1 in HBV replication.Scientific reports · 2021Article
- The Hepatitis B Virus Interactome: A Comprehensive Overview.Frontiers in microbiology · 2021Review
- Bone morphogenetic protein 4 provides cancer-supportive phenotypes to liver fibroblasts in patients with hepatocellular carcinoma.Journal of gastroenterology · 2019Article
- RETRACTED: HBV-encoded miR-2 functions as an oncogene by downregulating TRIM35 but upregulating RAN in liver cancer cells.EBioMedicine · 2019Article
- Regulation of the Hepatitis B virus replication and gene expression by the multi-functional protein TARDBP.Scientific reports · 2019Article
- USP15 Participates in Hepatitis C Virus Propagation through Regulation of Viral RNA Translation and Lipid Droplet Formation.Journal of virology · 2019Article
- Peroxiredoxin 1, a Novel HBx-Interacting Protein, Interacts with Exosome Component 5 and Negatively Regulates Hepatitis B Virus (HBV) Propagation through Degradation of HBV RNA.Journal of virology · 2019Article
- Characterization of miR-122-independent propagation of HCV.PLoS pathogens · 2017Article
- The current status and future directions of hepatitis B antiviral drug discovery.Expert opinion on drug discovery · 2017Review
- Depletion of JMJD5 sensitizes tumor cells to microtubule-destabilizing agents by altering microtubule stability.Cell cycle (Georgetown, Tex.) · 2016Article
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Authors and funding
20 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
unlabelledHepatitis B virus (HBV) is a causative agent for chronic liver diseases such as hepatitis, cirrhosis, and hepatocellular carcinoma (HCC). HBx protein encoded by the HBV genome plays crucial roles not only in pathogenesis but also in replication of HBV. Although HBx has been shown to bind to a number of host proteins, the molecular mechanisms by which HBx regulates HBV replication are largely unknown. In this study, we identified jumonji C-domain-containing 5 (JMJD5) as a novel binding partner of HBx interacting in the cytoplasm. DNA microarray analysis revealed that JMJD5-knockout (JMJD5KO) Huh7 cells exhibited a significant reduction in the expression of transcriptional factors involved in hepatocyte differentiation, such as HNF4A, CEBPA, and FOXA3. We found that hydroxylase activity of JMJD5 participates in the regulation of these transcriptional factors. Moreover, JMJD5KO Huh7 cells exhibited a severe reduction in HBV replication, and complementation of HBx expression failed to rescue replication of a mutant HBV deficient in HBx, suggesting that JMJD5 participates in HBV replication through an interaction with HBx. We also found that replacing Gly(135) with Glu in JMJD5 abrogates binding with HBx and replication of HBV. Moreover, the hydroxylase activity of JMJD5 was crucial for HBV replication. Collectively, these results suggest that direct interaction of JMJD5 with HBx facilitates HBV replication through the hydroxylase activity of JMJD5. IMPORTANCE: HBx protein encoded by hepatitis B virus (HBV) plays important roles in pathogenesis and replication of HBV. We identified jumonji C-domain-containing 5 (JMJD5) as a novel binding partner to HBx. JMJD5 was shown to regulate several transcriptional factors to maintain hepatocyte function. Although HBx had been shown to support HBV replication, deficiency of JMJD5 abolished contribution of HBx in HBV replication, suggesting that HBx-mediated HBV replication is largely dependent on JMJD5. We showed that hydroxylase activity of JMJD5 in the C terminus region is crucial for expression of HNF4A and replication of HBV. Furthermore, a mutant JMJD5 with Gly(135) replaced by Glu failed to interact with HBx and to rescue the replication of HBV in JMJD5-knockout cells. Taken together, our data suggest that interaction of JMJD5 with HBx facilitates HBV replication through the hydroxylase activity of JMJD5.
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