Evidence map›Paper›PMID 24137500›Full record

ArticlePloS one2013

Sphingosine kinase 1 serves as a pro-viral factor by regulating viral RNA synthesis and nuclear export of viral ribonucleoprotein complex upon influenza virus infection.

Young-Jin Seo, Curtis J Pritzl, Madhuvanthi Vijayan, Kavita Bomb, Mariah E McClain, Stephen Alexander, Bumsuk Hahm

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

53 citing papers in PubMed, 84 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Review
  8. The Implication of Sphingolipids in Viral Infections.International journal of molecular sciences · 2023
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Dyslipidemia in breast cancer patients increases the risk of SAR-CoV-2 infection.Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases · 2021
    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

7 authors at 1 institution in 1 country.

Young-Jin SeoDepartments of Surgery & Molecular Microbiology and Immunology, University of Missouri-Columbia, Columbia, Missouri, United States of America.
Curtis J Pritzl
Madhuvanthi Vijayan
Kavita Bomb
Mariah E McClain
Stephen Alexander
Bumsuk Hahm
University of Missouri · US

Funding

Control of influenza virus by sphingolipid metabolismR01AI091797 · NIAID · UNIVERSITY OF MISSOURI-COLUMBIA · PI HAHM, BUMSUK · 2011 to 2015
$1.8M
Novel modulation of dendritic cell response against a chronic virus infectionR21AI088363 · NIAID · UNIVERSITY OF MISSOURI-COLUMBIA · PI HAHM, BUMSUK · 2010 to 2011
$389k
NIAID NIH HHS R01 AI091797NIAID NIH HHS R01AI091797NIAID NIH HHS R21 AI088363NIAID NIH HHS R21AI088363
6 · The paper itself

Abstract

Influenza continues to pose a threat to humans by causing significant morbidity and mortality. Thus, it is imperative to investigate mechanisms by which influenza virus manipulates the function of host factors and cellular signal pathways. In this study, we demonstrate that influenza virus increases the expression and activation of sphingosine kinase (SK) 1, which in turn regulates diverse cellular signaling pathways. Inhibition of SK suppressed virus-induced NF-κB activation and markedly reduced the synthesis of viral RNAs and proteins. Further, SK blockade interfered with activation of Ran-binding protein 3 (RanBP3), a cofactor of chromosome region maintenance 1 (CRM1), to inhibit CRM1-mediated nuclear export of the influenza viral ribonucleoprotein complex. In support of this observation, SK inhibition altered the phosphorylation of ERK, p90RSK, and AKT, which is the upstream signal of RanBP3/CRM1 activation. Collectively, these results indicate that SK is a key pro-viral factor regulating multiple cellular signal pathways triggered by influenza virus infection.

Indexed as

Active Transport, Cell NucleusAnimalsCell NucleusDogsEnzyme ActivationEnzyme InhibitorsHEK293 CellsHumansInfluenza A Virus, H1N1 SubtypeInfluenza A Virus, H3N2 SubtypeMadin Darby Canine Kidney CellsMAP Kinase Signaling SystemNF-kappa BNuclear ProteinsNucleocytoplasmic Transport ProteinsPhosphorylationEnzyme InhibitorsNF-kappa BNuclear ProteinsNucleocytoplasmic Transport ProteinsPhosphotransferases (Alcohol Group Acceptor)RANBP3 protein, humanRibonucleoproteinsRNA, ViralSphingosine KinaseViral Proteins

Identifiers

PMID24137500
PMCPMC3796690
OpenAlexW2038047011

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.