ArticleJournal of virology2008
The FUSE binding protein is a cellular factor required for efficient replication of hepatitis C virus.
Article in Journal of virology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
29 citing papers in PubMed, 55 citations in OpenAlex.
- FUBP3 regulates expression and alternative splicing of genes associated with cell proliferation and apoptosis in cancer cells.Oncology letters · 2026Article
- Review
- FBP1 knockdown decreases ovarian cancer formation and cisplatin resistance through EZH2-mediated H3K27me3.Bioscience reports · 2022Article
- FUSE binding protein FUBP3 is a potent regulator in Japanese encephalitis virus infection.Virology journal · 2021Article
- Comparative structural analyses and nucleotide-binding characterization of the four KH domains of FUBP1.Scientific reports · 2020Article
- NORAD orchestrates endometrial cancer progression by sequestering FUBP1 nuclear localization to promote cell apoptosis.Cell death & disease · 2020Article
- The master regulator FUBP1: its emerging role in normal cell function and malignant development.Cellular and molecular life sciences : CMLS · 2019Review
- Tylophorine Analogs Allosterically Regulates Heat Shock Cognate Protein 70 And Inhibits Hepatitis C Virus Replication.Scientific reports · 2017Article
- Article
- Article
- Additive Promotion of Viral Internal Ribosome Entry Site-Mediated Translation by Far Upstream Element-Binding Protein 1 and an Enterovirus 71-Induced Cleavage Product.PLoS pathogens · 2016Article
- Staufen1 promotes HCV replication by inhibiting protein kinase R and transporting viral RNA to the site of translation and replication in the cells.Nucleic acids research · 2016Article
- FUSE Binding Protein 1 Facilitates Persistent Hepatitis C Virus Replication in Hepatoma Cells by Regulating Tumor Suppressor p53.Journal of virology · 2015Article
- Fuse binding protein antagonizes the transcription activity of tumor suppressor protein p53.BMC cancer · 2014Article
- Autophagy in hepatitis C virus-host interactions: potential roles and therapeutic targets for liver-associated diseases.World journal of gastroenterology · 2014Review
- Update on the Development of Anti-Viral Agents Against Hepatitis C.Journal of clinical and translational hepatology · 2013Review
- Far upstream element-binding protein 1 and RNA secondary structure both mediate second-step splicing repression.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Far upstream element binding protein 1: a commander of transcription, translation and beyond.Oncogene · 2013Review
- Affinity capture and identification of host cell factors associated with hepatitis C virus (+) strand subgenomic RNA.Molecular & cellular proteomics : MCP · 2013Article
- Low oxygen tension enhances hepatitis C virus replication.Journal of virology · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatitis C virus (HCV) infection is the leading cause of liver cirrhosis and hepatocellular carcinoma and one of the primary indications for liver transplantation. The molecular mechanisms underlying the actions of host factors in HCV replication remain poorly defined. FUSE (far upstream element of the c-myc proto-oncogene) binding protein (FBP) is a cellular factor that we have identified as a binder of HCV 3' nontranslated region (3'NTR). Mapping of the binding site showed that FBP specifically interacts with the poly(U) tract within the poly(U/UC) region of the 3'NTR. Silencing of FBP expression by small interfering RNA in cells carrying HCV subgenomic replicons severely reduced viral replication, while overexpression of FBP significantly enhanced viral replication. We confirmed these observations by an in vitro HCV replication assay in the cell-free replicative lysate, which suggested that there is a direct correlation between the cellular FBP level and HCV replication. FBP immunoprecipitation coprecipitated HCV nonstructural protein 5A (NS5A), indicating that FBP interacts with HCV NS5A, which is known to function as a link between HCV translation and replication. Although FBP is mainly localized in the nucleus, we found that in MH14 cells a significant level of this protein is colocalized with NS5A in the cytosol, a site of HCV replication. While the mechanism of FBP involvement in HCV replication is yet to be delineated, our findings suggest that it may be an important regulatory component that is essential for efficient replication of HCV.
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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.