Evidence map›Paper›PMID 30038017›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2018

RNA triphosphatase DUSP11 enables exonuclease XRN-mediated restriction of hepatitis C virus.

Rodney P Kincaid, Victor L Lam, Rachel P Chirayil, Glenn Randall, Christopher S Sullivan

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
3.0field-weighted citation impact, top 7% 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

32 citing papers in PubMed, 41 citations in OpenAlex.

  1. Article
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  7. Article
  8. Review
  9. Article
  10. Subversion of a protein-microRNA signaling pathway by hepatitis C virus.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Dual-Specificity Phosphatases and Kidney Diseases.Kidney diseases (Basel, Switzerland) · 2022
    Review
  16. Article
  17. Article
  18. miR-122-based therapies select for three distinct resistance mechanisms based on alterations in RNA structure.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  19. Review
  20. 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

5 authors at 2 institutions in 1 country.

Rodney P KincaidCenter for Systems and Synthetic Biology, Department of Molecular Biosciences, The University of Texas at Austin, Austin, TX 78712-0162.
Victor L LamCenter for Systems and Synthetic Biology, Department of Molecular Biosciences, The University of Texas at Austin, Austin, TX 78712-0162.
Rachel P ChirayilCenter for Systems and Synthetic Biology, Department of Molecular Biosciences, The University of Texas at Austin, Austin, TX 78712-0162.
Glenn RandallDepartment of Microbiology, The University of Chicago, Chicago, IL 60637.
Christopher S SullivanCenter for Systems and Synthetic Biology, Department of Molecular Biosciences, The University of Texas at Austin, Austin, TX 78712-0162; chris_sullivan@austin.utexas.edu.
The University of Texas at Austin · USUniversity of Chicago · US

Funding

Elucidating How Tri-phosphatase DUSP11 Controls HCV Infection and Hepatocyte InflammationR01AI134980 · NIAID · UNIVERSITY OF TEXAS AT AUSTIN · PI RANDALL, GLENN C, SULLIVAN, CHRISTOPHER S. · 2018 to 2021
$1.8M
HEPATOCYTE REMODELING BY HEPATITIS C VIRUSR01DK102883 · NIDDK · UNIVERSITY OF CHICAGO · PI RANDALL, GLENN C · 2015 to 2018
$1.4M
NIDDK NIH HHS R01 DK102883
6 · The paper itself

Abstract

Seventy percent of people infected with hepatitis C virus (HCV) will suffer chronic infection, putting them at risk for liver disease, including hepatocellular carcinoma. The full range of mechanisms that render some people more susceptible to chronic infection and liver disease is still being elucidated. XRN exonucleases can restrict HCV replication and may help to resolve HCV infections. However, it is unknown how 5' triphosphorylated HCV transcripts, primary products of the viral polymerase, become susceptible to attack by 5' monophosphate-specific XRNs. Here, we show that the 5' RNA triphosphatase DUSP11 acts on HCV transcripts, rendering them susceptible to XRN-mediated attack. Cells lacking DUSP11 show substantially enhanced HCV replication, and this effect is diminished when XRN expression is reduced. MicroRNA-122 (miR-122), a target of current phase II anti-HCV drugs, is known to protect HCV transcripts against XRNs. We show that HCV replication is less dependent on miR-122 in cells lacking DUSP11. Combined, these results implicate DUSP11 as an important component of XRN-mediated restriction of HCV.

Indexed as

Acid Anhydride HydrolasesCarcinoma, HepatocellularCell Line, TumorDual-Specificity PhosphatasesExoribonucleasesGene Knockout TechniquesGenome, ViralHepacivirusHepatitis C, ChronicHepatocytesHost-Pathogen InteractionsHumansLiver NeoplasmsMicroRNAsRNA, Small InterferingRNA, ViralAcid Anhydride HydrolasesDual-Specificity PhosphatasesDUSP11 protein, humanExoribonucleasesMicroRNAsMIRN122 microRNA, humanRNA, Small InterferingRNA triphosphataseRNA, ViralmicroRNAmiR-122restriction factor

Identifiers

PMID30038017
PMCPMC6094126
OpenAlexW2883555730

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.