Evidence map›Paper›PMID 30996098›Full record

ArticleJournal of virology2019

Phosphoproteome Analysis of Cells Infected with Adapted and Nonadapted Influenza A Virus Reveals Novel Pro- and Antiviral Signaling Networks.

Axel Weber, Sharmistha Dam, Vera V Saul, Irina Kuznetsova, Christin Müller, Karin Fritz-Wolf, Katja Becker, Uwe Linne, Hongbo Gu, Matthew P Stokes and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.2field-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

17 citing papers in PubMed, 26 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Viral Modulation of Host Splicing.Annual review of virology · 2025
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Review
  16. Article
  17. Article
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

13 authors at 4 institutions in 2 countries.

Axel Weber *Rudolf Buchheim Institute of Pharmacology, Justus Liebig University Giessen, Giessen, Germany.
Sharmistha Dam *Institute of Biochemistry, Justus Liebig University, Giessen, Germany.
Vera V SaulInstitute of Biochemistry, Justus Liebig University, Giessen, Germany.
Irina KuznetsovaInstitute of Medical Virology, Justus Liebig University Giessen, Giessen, Germany.
Christin MüllerInstitute of Medical Virology, Justus Liebig University Giessen, Giessen, Germany.
Karin Fritz-WolfMax Planck Institute for Medical Research, Heidelberg, Germany.
Katja BeckerBiochemistry and Molecular Biology, Justus Liebig University, Giessen, Germany.
Uwe LinneMass spectrometry facility of the Department of Chemistry, Philipps-Universität Marburg, Marburg, Germany.
Hongbo GuCell Signaling Technology, Danvers, Massachusetts, USA.
Matthew P StokesCell Signaling Technology, Danvers, Massachusetts, USA.
Stephan PleschkaInstitute of Medical Virology, Justus Liebig University Giessen, Giessen, Germany.
Michael KrachtRudolf Buchheim Institute of Pharmacology, Justus Liebig University Giessen, Giessen, Germany Michael.Kracht@pharma.med.uni-giessen.de Lienhard.Schmitz@biochemie.med.uni-giessen.de.
M Lienhard SchmitzInstitute of Biochemistry, Justus Liebig University, Giessen, Germany Michael.Kracht@pharma.med.uni-giessen.de Lienhard.Schmitz@biochemie.med.uni-giessen.de.
Justus-Liebig-Universität Gießen · DECell Signaling Technology (United States) · USGerman Center for Lung Research · DEPhilipps University of Marburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Influenza A viruses (IAVs) quickly adapt to new environments and are well known to cross species barriers. To reveal a molecular basis for these phenomena, we compared the Ser/Thr and Tyr phosphoproteomes of murine lung epithelial cells early and late after infection with mouse-adapted SC35M virus or its nonadapted SC35 counterpart. With this analysis we identified a large set of upregulated Ser/Thr phosphorylations common to both viral genotypes, while Tyr phosphorylations showed little overlap. Most of the proteins undergoing massive changes of phosphorylation in response to both viruses regulate chromatin structure, RNA metabolism, and cell adhesion, including a focal adhesion kinase (FAK)-regulated network mediating the regulation of actin dynamics. IAV also affected phosphorylation of activation loops of 37 protein kinases, including FAK and several phosphatases, many of which were not previously implicated in influenza virus infection. Inhibition of FAK proved its contribution to IAV infection. Novel phosphorylation sites were found on IAV-encoded proteins, and the functional analysis of selected phosphorylation sites showed that they either support (NA Ser178) or inhibit (PB1 Thr223) virus propagation. Together, these data allow novel insights into IAV-triggered regulatory phosphorylation circuits and signaling networks.

Indexed as

AnimalsAntiviral AgentsCell LineFocal Adhesion Protein-Tyrosine KinasesGenomeHost-Pathogen InteractionsHumansInfluenza A virusMiceModels, MolecularOrthomyxoviridae InfectionsPhosphorylationProtein ConformationProteomeSignal TransductionViral ProteinsAntiviral AgentsFocal Adhesion Protein-Tyrosine KinasesProteomeViral Proteinsinfluenzakinasephosphoproteomesignaling network

Identifiers

PMID30996098
PMCPMC6580974
OpenAlexW2938408743

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.