Evidence map›Paper›PMID 31004050›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2019

MAPK pathway and B cells overactivation in multiple sclerosis revealed by phosphoproteomics and genomic analysis.

Ekaterina Kotelnikova, Narsis A Kiani, Dimitris Messinis, Inna Pertsovskaya, Vicky Pliaka, Marti Bernardo-Faura, Melanie Rinas, Gemma Vila, Irati Zubizarreta, Irene Pulido-Valdeolivas and 13 more

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
5.5field-weighted citation impact, top 3% 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

24 citing papers in PubMed, 61 citations in OpenAlex.

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  8. Multiscale networks in multiple sclerosis.PLoS computational biology · 2024
    Article
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  11. Article
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  15. Proteomics in Multiple Sclerosis: The Perspective of the Clinician.International journal of molecular sciences · 2022
    Review
  16. Article
  17. Article
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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

23 authors at 11 institutions in 8 countries.

Ekaterina KotelnikovaCenter of Neuroimmunology, Institut d'Investigacions Biomèdiques August Pi Sunyer, Barcelona 08036, Spain.
Narsis A KianiUnit of Computational Medicine, Department of Medicine, Karolinska Institutet, Solna, Stockholm SE-171 76, Sweden.
Dimitris MessinisProtatOnce, Athens 15343, Greece.
Inna PertsovskayaCenter of Neuroimmunology, Institut d'Investigacions Biomèdiques August Pi Sunyer, Barcelona 08036, Spain.
Vicky PliakaProtatOnce, Athens 15343, Greece.
Marti Bernardo-FauraEuropean Bioinformatics Institute, European Molecular Biology Laboratory, Hinxton CB10 1SD, United Kingdom.ORCID 0000-0002-8023-3263
Melanie RinasJoint Research Centre for Computational Biomedicine, Rheinisch-Westfälische Technische Hochschule - Aachen University Hospital, Aachen 52074, Germany.
Gemma VilaCenter of Neuroimmunology, Institut d'Investigacions Biomèdiques August Pi Sunyer, Barcelona 08036, Spain.
Irati ZubizarretaCenter of Neuroimmunology, Institut d'Investigacions Biomèdiques August Pi Sunyer, Barcelona 08036, Spain.
Irene Pulido-ValdeolivasCenter of Neuroimmunology, Institut d'Investigacions Biomèdiques August Pi Sunyer, Barcelona 08036, Spain.
Theodore SakellaropoulosDepartment of Mechanical Engineering, National Technical University of Athens, Athens 15780, Greece.
Wolfgang FaigleDepartment of Neurology, University of Zurich, Zurich 8091, Switzerland.
Gilad SilberbergUnit of Computational Medicine, Department of Medicine, Karolinska Institutet, Solna, Stockholm SE-171 76, Sweden.
Mar MassoBionure Farma SL, Barcelona 08028, Spain.
Pernilla StridhDepartment of Neurology, Karolinska University Hospital, Stockholm SE-171 77, Sweden.
Janina BehrensNeuroCure Clinical Research Center, Charité University Universitätsmedizin Berlin, Berlin 13125, Germany.
Tomas OlssonDepartment of Neurology, Karolinska University Hospital, Stockholm SE-171 77, Sweden.
Roland MartinDepartment of Neurology, University of Zurich, Zurich 8091, Switzerland.
Friedemann PaulNeuroCure Clinical Research Center, Charité University Universitätsmedizin Berlin, Berlin 13125, Germany.
Leonidas G AlexopoulosProtatOnce, Athens 15343, Greece.
Julio Saez-RodriguezEuropean Bioinformatics Institute, European Molecular Biology Laboratory, Hinxton CB10 1SD, United Kingdom.
Jesper TegnerUnit of Computational Medicine, Department of Medicine, Karolinska Institutet, Solna, Stockholm SE-171 76, Sweden.
Pablo VillosladaCenter of Neuroimmunology, Institut d'Investigacions Biomèdiques August Pi Sunyer, Barcelona 08036, Spain; pvilloslada@clinic.ub.es.ORCID 0000-0002-8735-6119
Consorci Institut D'Investigacions Biomediques August Pi I Sunyer · ESNational Technical University of Athens · GREuropean Bioinformatics Institute · GBKarolinska Institutet · SEKarolinska University Hospital · SEUniversity of Zurich · CHCharité - Universitätsmedizin Berlin · DEInstitute for Information Transmission Problems · RUMax Delbrück Center · DEScience for Life Laboratory · SEUniversitätsklinikum Aachen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dysregulation of signaling pathways in multiple sclerosis (MS) can be analyzed by phosphoproteomics in peripheral blood mononuclear cells (PBMCs). We performed in vitro kinetic assays on PBMCs in 195 MS patients and 60 matched controls and quantified the phosphorylation of 17 kinases using xMAP assays. Phosphoprotein levels were tested for association with genetic susceptibility by typing 112 single-nucleotide polymorphisms (SNPs) associated with MS susceptibility. We found increased phosphorylation of MP2K1 in MS patients relative to the controls. Moreover, we identified one SNP located in the PHDGH gene and another on IRF8 gene that were associated with MP2K1 phosphorylation levels, providing a first clue on how this MS risk gene may act. The analyses in patients treated with disease-modifying drugs identified the phosphorylation of each receptor's downstream kinases. Finally, using flow cytometry, we detected in MS patients increased STAT1, STAT3, TF65, and HSPB1 phosphorylation in CD19

Indexed as

B-LymphocytesMultiple SclerosisPhosphoproteinsPolymorphism, Single NucleotideProteomicsCell ProliferationCell SurvivalFemaleHumansMaleMAP Kinase Signaling SystemPhosphorylationProtein KinasesPhosphoproteinsProtein KinasesautoimmunityB cellsmultiple sclerosisphosphoproteomicssignaling pathways

Identifiers

PMID31004050
PMCPMC6510997
OpenAlexW2939980218

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.