Evidence map›Paper›PMID 22993150›Full record

ArticleJournal of virology2012

Hepatitis C virus infection suppresses GLUT2 gene expression via downregulation of hepatocyte nuclear factor 1α.

Chieko Matsui, Ikuo Shoji, Shusaku Kaneda, Imelda Rosalyn Sianipar, Lin Deng, Hak Hotta

Open access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.8field-weighted citation impact, top 15% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

23 citing papers in PubMed, 48 citations in OpenAlex.

  1. Article
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  7. Article
  8. HCV affects KEndocrine · 2024
    Article
  9. Article
  10. Review
  11. Article
  12. The Role of Chaperone-Mediated Autophagy in Hepatitis C Virus-Induced Pathogenesis.Frontiers in cellular and infection microbiology · 2021
    Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 2 countries.

Chieko MatsuiDivision of Microbiology, Center for Infectious Diseases, Kobe University Graduate School of Medicine, Chuo-ku, Kobe, Hyogo, Japan.
Ikuo Shoji
Shusaku Kaneda
Imelda Rosalyn Sianipar
Lin Deng
Hak Hotta
Kobe University · JPUniversity of Indonesia · ID

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatitis C virus (HCV) infection causes not only intrahepatic diseases but also extrahepatic manifestations, including type 2 diabetes. We previously reported that HCV replication suppresses cellular glucose uptake by downregulation of cell surface expression of glucose transporter 2 (GLUT2) (D. Kasai et al., J. Hepatol. 50:883-894, 2009). GLUT2 mRNA levels were decreased in both HCV RNA replicon cells and HCV J6/JFH1-infected cells. To elucidate molecular mechanisms of HCV-induced suppression of GLUT2 gene expression, we analyzed transcriptional regulation of the GLUT2 promoter using a series of GLUT2 promoter-luciferase reporter plasmids. HCV-induced suppression of GLUT2 promoter activity was abrogated when the hepatocyte nuclear factor 1α (HNF-1α)-binding motif was deleted from the GLUT2 promoter. HNF-1α mRNA levels were significantly reduced in HCV J6/JFH1-infected cells. Furthermore, HCV infection remarkably decreased HNF-1α protein levels. We assessed the effects of proteasome inhibitor or lysosomal protease inhibitors on the HCV-induced reduction of HNF-1α protein levels. Treatment of HCV-infected cells with a lysosomal protease inhibitor, but not with a proteasome inhibitor, restored HNF-1α protein levels, suggesting that HCV infection promotes lysosomal degradation of HNF-1α protein. Overexpression of NS5A protein enhanced lysosomal degradation of HNF-1α protein and suppressed GLUT2 promoter activity. Immunoprecipitation analyses revealed that the region from amino acids 1 to 126 of the NS5A domain I physically interacts with HNF-1α protein. Taken together, our results suggest that HCV infection suppresses GLUT2 gene expression via downregulation of HNF-1α expression at transcriptional and posttranslational levels. HCV-induced downregulation of HNF-1α expression may play a crucial role in glucose metabolic disorders caused by HCV.

Indexed as

Analysis of VarianceAntibodies, MonoclonalCell Line, TumorDNA PrimersGene Expression RegulationGlucoseGlucose Transporter Type 2Hepatitis CHepatocyte Nuclear Factor 1-alphaHumansImmunoblottingImmunoprecipitationLuciferasesLysosomesPlasmidsPromoter Regions, GeneticAntibodies, MonoclonalDNA PrimersGlucoseGlucose Transporter Type 2Hepatocyte Nuclear Factor 1-alphaLuciferasesNS-5 protein, hepatitis C virusRNA-Dependent RNA PolymeraseSLC2A2 protein, humanViral Nonstructural Proteins

Identifiers

PMID22993150
PMCPMC3497665
OpenAlexW2150802339

What OpenQuestion holds

Textmetadata
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Registered trials

None linked

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.