Evidence map›Paper›PMID 24997996›Full record

ArticleMolecular & cellular proteomics : MCP2014

Phosphoproteomics combined with quantitative 14-3-3-affinity capture identifies SIRT1 and RAI as novel regulators of cytosolic double-stranded RNA recognition pathway.

Tiina Öhman, Sandra Söderholm, Petteri Hintsanen, Elina Välimäki, Niina Lietzén, Carol MacKintosh, Tero Aittokallio, Sampsa Matikainen, Tuula A Nyman

Open access · hybridAbstract read
In one paragraph

Article in Molecular & cellular proteomics : MCP, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.0field-weighted citation impact, top 24% 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

5 citing papers in PubMed, 10 citations in OpenAlex.

  1. 14-3-3ζ-TRAF5 axis governs interleukin-17A signaling.Proceedings of the National Academy of Sciences of the United States of America · 2020
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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

9 authors at 4 institutions in 2 countries.

Tiina ÖhmanFrom the ‡Institute of Biotechnology, FI-00014 University of Helsinki, Helsinki, Finland;
Sandra SöderholmFrom the ‡Institute of Biotechnology, FI-00014 University of Helsinki, Helsinki, Finland; §Finnish Institute of Occupational Health, FI-00250 Helsinki, Finland;
Petteri Hintsanen¶Institute for Molecular Medicine Finland (FIMM), FI-00014 University of Helsinki, Helsinki, Finland;
Elina VälimäkiFrom the ‡Institute of Biotechnology, FI-00014 University of Helsinki, Helsinki, Finland; §Finnish Institute of Occupational Health, FI-00250 Helsinki, Finland;
Niina LietzénFrom the ‡Institute of Biotechnology, FI-00014 University of Helsinki, Helsinki, Finland;
Carol MacKintosh**University of Dundee, Dundee, Scotland DD1 5EH, United Kingdom.
Tero Aittokallio¶Institute for Molecular Medicine Finland (FIMM), FI-00014 University of Helsinki, Helsinki, Finland;
Sampsa Matikainen§Finnish Institute of Occupational Health, FI-00250 Helsinki, Finland;
Tuula A NymanFrom the ‡Institute of Biotechnology, FI-00014 University of Helsinki, Helsinki, Finland; tuula.nyman@helsinki.fi.
University of Helsinki · FIFinnish Institute of Occupational Health · FIHelsinki Institute of Physics · FIUniversity of Dundee · GB

Funding

Medical Research Council MC_EX_G0801767
6 · The paper itself

Abstract

Viral double-stranded RNA (dsRNA) is the most important viral structure recognized by cytosolic pattern-recognition receptors of the innate immune system, and its recognition results in the activation of signaling cascades that stimulate the production of antiviral cytokines and apoptosis of infected cells. 14-3-3 proteins are ubiquitously expressed regulatory molecules that participate in a variety of cellular processes, and 14-3-3 protein-mediated signaling pathways are activated by cytoplasmic dsRNA in human keratinocytes. However, the functional role of 14-3-3 protein-mediated interactions during viral dsRNA stimulation has remained uncharacterized. Here, we used functional proteomics to identify proteins whose phosphorylation and interaction with 14-3-3 is modulated by dsRNA and to characterize the signaling pathways activated during cytosolic dsRNA-induced innate immune response in human HaCaT keratinocytes. Phosphoproteome analysis showed that several MAPK- and immune-response-related signaling pathways were activated after dsRNA stimulation. Interactome analysis identified RelA-associated inhibitor, high-mobility group proteins, and several proteins associated with host responses to viral infection as novel 14-3-3 target proteins. Functional studies showed that RelA-associated inhibitor regulated dsRNA-induced apoptosis and TNF production. Integrated network analyses of proteomic data revealed that sirtuin1 was a central molecule regulated by 14-3-3s during dsRNA stimulation. Further experiments showed that sirtuin 1 negatively regulated dsRNA-induced NFκB transcriptional activity, suppressed expression of antiviral cytokines, and protected cells from apoptosis in dsRNA-stimulated and encephalomyocarditis-virus-infected keratinocytes. In conclusion, our data highlight the importance of 14-3-3 proteins in antiviral responses and identify RelA-associated inhibitor and sirtuin 1 as novel regulators of antiviral innate immune responses.

Indexed as

14-3-3 ProteinsCardiovirus InfectionsCell LineCytosolEncephalomyocarditis virusHumansImmunity, InnateIntracellular Signaling Peptides and ProteinsKeratinocytesPhosphorylationProteomicsRepressor ProteinsRNA, Double-StrandedRNA, ViralSignal TransductionSirtuin 114-3-3 ProteinsIntracellular Signaling Peptides and ProteinsPPP1R13L protein, humanRepressor ProteinsRNA, Double-StrandedRNA, ViralSIRT1 protein, humanSirtuin 1

Identifiers

PMID24997996
PMCPMC4188990
OpenAlexW2144991158

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.