Evidence map›Paper›PMID 17991716›Full record

ArticleThe American journal of pathology2007

Responses of nontransformed human hepatocytes to conditional expression of full-length hepatitis C virus open reading frame.

Weiliang Tang, Catherine A Lázaro, Jean S Campbell, W Tony Parks, Michael G Katze, Nelson Fausto

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

18 citing papers in PubMed, 28 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Signaling Induced by Chronic Viral Hepatitis: Dependence and Consequences.International journal of molecular sciences · 2022
    Review
  5. Review
  6. Review
  7. Article
  8. Review
  9. Article
  10. Hepatitis C virus proteins modulate microRNA expression and chemosensitivity in malignant hepatocytes.Clinical cancer research : an official journal of the American Association for Cancer Research · 2010
    Article
  11. Roles for endocytic trafficking and phosphatidylinositol 4-kinase III alpha in hepatitis C virus replication.Proceedings of the National Academy of Sciences of the United States of America · 2009
    Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Virogenomics: the virus-host interaction revisited.Current opinion in microbiology · 2008
    Review
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 1 institution in 1 country.

Weiliang TangDepartment of Pathology, University of Washington School of Medicine, K078 Health Sciences Building, Box 357705, Seattle, WA 98195-7705, USA.
Catherine A Lázaro
Jean S Campbell
W Tony Parks
Michael G Katze
Nelson Fausto
University of Washington · US

Funding

Pathogenesis of Hepatocellular CarcinomasR01CA074131 · NCI · UNIVERSITY OF WASHINGTON · PI FAUSTO, NELSON · 1997 to 2010
$3.1M
NCI NIH HHS CA 074131NCI NIH HHS CA074131NCI NIH HHS R01 CA074131NIAID NIH HHS U19 AI 148214NIAID NIH HHS U19 AI148214NIDA NIH HHS P30 DA01562501
6 · The paper itself

Abstract

Hepatitis C virus (HCV) is a major cause of chronic hepatitis that can lead to cirrhosis and hepatocellular carcinoma. To study the effects of HCV protein expression on host cells, we established conditional expression of the full-length open reading frame (ORF) of an infectious cDNA clone of HCV (genotype 1a, H77 strain) in the nontransformed human hepatocyte line cell HH4 using the ecdysone receptor regulatory system. Treatment with the ecdysone analog ponasterone-A induced tightly regulated and dose-dependent full-length HCV ORF expression and properly processed HCV proteins. HCV Core, NS3, and NS5A colocalized in perinuclear regions and associated with the early endosomal protein EEA1. HCV ORF expression caused marked growth inhibition, increased intracellular reactive oxygen species, up-regulation of glutamate-l-cysteine ligase activity, increased glutathione level, and activation of nuclear factor kappaB. Although it was not directly cytotoxic, HCV ORF expression sensitized HH4 cells to Fas at certain concentrations but not to tumor necrosis factor-related apoptosis-inducing ligand. HCV ORF expression in HH4 cells up-regulated genes involved in innate immune response/inflammation and oxidative stress responses and down-regulated cell growth-related genes. Expression of HCV ORF in host cells may contribute to HCV pathogenesis by producing oxidative stress and increasing the expression of genes related to the innate immune response and inflammation.

Indexed as

ApoptosisCell AdhesionCell CycleCell ProliferationCell SurvivalEcdysteroneExtracellular Matrixfas ReceptorGene ExpressionGlutamate-Cysteine LigaseHepacivirusHepatocytesHumansImmunity, InnateNF-kappa BOligonucleotide Array Sequence AnalysisEcdysteronefas ReceptorGlutamate-Cysteine LigaseNF-kappa BPolyproteinsponasterone AViral Proteins

Identifiers

PMID17991716
PMCPMC2111107
OpenAlexW1997530090

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.