Evidence map›Paper›PMID 25993413›Full record

ArticlePloS one2015

Label-Free Protein-RNA Interactome Analysis Identifies Khsrp Signaling Downstream of the p38/Mk2 Kinase Complex as a Critical Modulator of Cell Cycle Progression.

Jorge Boucas, Christian Fritz, Anna Schmitt, Arina Riabinska, Lisa Thelen, Martin Peifer, Uschi Leeser, Peter Nuernberg, Janine Altmueller, Matthias Gaestel and 2 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

25 citing papers in PubMed, 37 citations in OpenAlex.

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  12. The Integrated RNA Landscape of Renal Preconditioning against Ischemia-Reperfusion Injury.Journal of the American Society of Nephrology : JASN · 2020
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  16. A brave new world of RNA-binding proteins.Nature reviews. Molecular cell biology · 2018
    Review
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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

12 authors at 3 institutions in 1 country.

Jorge BoucasDepartment I of Internal Medicine, University Hospital of Cologne, Weyertal 115B, 50931, Cologne, Germany; Cologne Excellence Cluster on Cellular Stress Response in Aging-Associated Diseases, University of Cologne, Weyertal 115B, 50931, Cologne, Germany.
Christian FritzDepartment I of Internal Medicine, University Hospital of Cologne, Weyertal 115B, 50931, Cologne, Germany; Cologne Excellence Cluster on Cellular Stress Response in Aging-Associated Diseases, University of Cologne, Weyertal 115B, 50931, Cologne, Germany.
Anna SchmittDepartment I of Internal Medicine, University Hospital of Cologne, Weyertal 115B, 50931, Cologne, Germany; Cologne Excellence Cluster on Cellular Stress Response in Aging-Associated Diseases, University of Cologne, Weyertal 115B, 50931, Cologne, Germany.
Arina RiabinskaDepartment I of Internal Medicine, University Hospital of Cologne, Weyertal 115B, 50931, Cologne, Germany; Cologne Excellence Cluster on Cellular Stress Response in Aging-Associated Diseases, University of Cologne, Weyertal 115B, 50931, Cologne, Germany.
Lisa ThelenDepartment I of Internal Medicine, University Hospital of Cologne, Weyertal 115B, 50931, Cologne, Germany; Cologne Excellence Cluster on Cellular Stress Response in Aging-Associated Diseases, University of Cologne, Weyertal 115B, 50931, Cologne, Germany.
Martin PeiferCenter for Molecular Medicine Cologne (CMMC), University of Cologne, Cologne, Germany; Department of Translational Genomics, University of Cologne, Cologne, Germany.
Uschi LeeserDepartment I of Internal Medicine, University Hospital of Cologne, Weyertal 115B, 50931, Cologne, Germany; Cologne Excellence Cluster on Cellular Stress Response in Aging-Associated Diseases, University of Cologne, Weyertal 115B, 50931, Cologne, Germany.
Peter NuernbergCologne Excellence Cluster on Cellular Stress Response in Aging-Associated Diseases, University of Cologne, Weyertal 115B, 50931, Cologne, Germany; Center for Molecular Medicine Cologne (CMMC), University of Cologne, Cologne, Germany; Cologne Center for Genomics (CCG), University of Cologne, Cologne, Germany.
Janine AltmuellerCologne Center for Genomics (CCG), University of Cologne, Cologne, Germany.
Matthias GaestelInstitute of Biochemistry, Hannover Medical School, Hannover, Germany.
Christoph DieterichComputational RNA Biology and Ageing, Max Planck Institute for Biology of Ageing, Joseph-Stelzmann Straße 9b, 50913, Cologne, Germany.
H Christian ReinhardtDepartment I of Internal Medicine, University Hospital of Cologne, Weyertal 115B, 50931, Cologne, Germany; Cologne Excellence Cluster on Cellular Stress Response in Aging-Associated Diseases, University of Cologne, Weyertal 115B, 50931, Cologne, Germany.
Max Planck Institute for Biology of Ageing · DEMedizinische Hochschule Hannover · DEUniversity of Cologne · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Growing evidence suggests a key role for RNA binding proteins (RBPs) in genome stability programs. Additionally, recent developments in RNA sequencing technologies, as well as mass-spectrometry techniques, have greatly expanded our knowledge on protein-RNA interactions. We here use full transcriptome sequencing and label-free LC/MS/MS to identify global changes in protein-RNA interactions in response to etoposide-induced genotoxic stress. We show that RBPs have distinct binding patterns in response to genotoxic stress and that inactivation of the RBP regulator module, p38/MK2, can affect the entire spectrum of protein-RNA interactions that take place in response to stress. In addition to validating the role of known RBPs like Srsf1, Srsf2, Elavl1 in the genotoxic stress response, we add a new collection of RBPs to the DNA damage response. We identify Khsrp as a highly regulated RBP in response to genotoxic stress and further validate its role as a driver of the G(1/)S transition through the suppression of Cdkn1a(P21) transcripts. Finally, we identify KHSRP as an indicator of overall survival, as well as disease free survival in glioblastoma multiforme.

Indexed as

AnimalsCells, CulturedCyclin-Dependent Kinase Inhibitor p21Disease-Free SurvivalDNA DamageELAV-Like Protein 1G1 Phase Cell Cycle CheckpointsGene Expression ProfilingGlioblastomaHumansIntracellular Signaling Peptides and ProteinsMAP-Kinase-Activated Kinase 2MiceNuclear Proteinsp38 Mitogen-Activated Protein KinasesProtein Serine-Threonine KinasesCyclin-Dependent Kinase Inhibitor p21Elavl1 protein, mouseELAV-Like Protein 1Intracellular Signaling Peptides and ProteinsKHSRP protein, humanMAP-Kinase-Activated Kinase 2Nuclear Proteinsp38 Mitogen-Activated Protein KinasesProtein Serine-Threonine KinasesRibonucleoproteinsRNARNA-Binding ProteinsSerine-Arginine Splicing FactorsSRSF2 protein, mouseTrans-Activators

Identifiers

PMID25993413
PMCPMC4439058
OpenAlexW1890105955

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.