ArticlePloS one2016
Hepatitis B Virus Stimulated Fibronectin Facilitates Viral Maintenance and Replication through Two Distinct Mechanisms.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
12 citing papers in PubMed, 13 citations in OpenAlex.
- Article
- The multifaceted roles of fibronectin in viral pathogenesis.Archives of virology · 2026Review
- Deciphering Autoantigen Signatures in Chikungunya Virus Infection Using Machine Learning: A Data-Driven Approach to Understand Host Immunity.Current microbiology · 2025Article
- Deciphering the phospho-signature induced by hepatitis B virus in primary human hepatocytes.Frontiers in microbiology · 2024Article
- Plasma Fibronectin as a Novel Predictor of Coronary Heart Disease: A Retrospective Study.Journal of cardiovascular development and disease · 2023Article
- Review
- Article
- Recent Progress on the Role of Fibronectin in Tumor Stromal Immunity and Immunotherapy.Current topics in medicinal chemistry · 2022Review
- Regulation of Pattern-Recognition Receptor Signaling by HBX During Hepatitis B Virus Infection.Frontiers in immunology · 2022Review
- Hepatitis B Surface Antigen Suppresses the Activation of Nuclear Factor Kappa B PathwayFrontiers in immunology · 2021Article
- Fibronectin Facilitates Enterovirus 71 Infection by Mediating Viral Entry.Journal of virology · 2018Article
- Inducible Rubicon facilitates viral replication by antagonizing interferon production.Cellular & molecular immunology · 2017Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fibronectin (FN) is a high molecular weight extracellular matrix protein that functions in cell adhesion, growth, migration, and embryonic development. However, little is known about the role of FN during viral infection. In the present study, we found significantly higher levels of FN in sera, and liver tissues from hepatitis B virus (HBV) patients relative to healthy individuals. HBV expression enhanced FN mRNA and protein levels in the hepatic cell lines Huh7 and HepG2. HBV infection of susceptible HepG2-sodium taurocholate co-transporting polypeptide cells also increased FN expression. We also found that transcriptional factor specificity protein 1 was involved in the induction of FN by HBV. Knockdown of FN expression significantly inhibited HBV DNA replication and protein synthesis through activating endogenous IFN-α production. In addition, FN interacted with the transforming growth factor β-activated protein kinase 1 (TAK1) and TAK1-binding protein complex and attenuated interferon signaling by inhibiting TAK1 phosphorylation. Furthermore, the nuclear translocation of NF-κB/p65 was found to be inhibited by FN. We also observed that FN promoted HBV enhancers to support HBV expression. These results suggest novel functions of endogenous FN involved in immune evasion and maintenance of HBV replication.
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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.