Evidence map›Paper›PMID 32314963›Full record

ArticleeLife2020

ERK3/MAPK6 controls IL-8 production and chemotaxis.

Katarzyna Bogucka, Malvika Pompaiah, Federico Marini, Harald Binder, Gregory Harms, Manuel Kaulich, Matthias Klein, Christian Michel, Markus P Radsak, Sebastian Rosigkeit and 3 more

Open access · goldAbstract read
In one paragraph

Article in eLife, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
2.1field-weighted citation impact, top 11% 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, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Intracellular pH regulates ubiquitin-mediated degradation of the MAP kinase ERK3.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  4. Article
  5. Atypical MAPKs in cancer.The FEBS journal · 2025
    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

13 authors at 4 institutions in 2 countries.

Katarzyna BoguckaCell Biology Unit, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany.
Malvika PompaiahCell Biology Unit, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany.
Federico MariniInstitute of Medical Biostatistics, Epidemiology and Informatics, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany.ORCID 0000-0003-3252-7758
Harald BinderInstitute of Medical Biostatistics, Epidemiology and Informatics, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany.
Gregory HarmsCell Biology Unit, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany.
Manuel KaulichGene Editing Group, Institute of Biochemistry II, Goethe University, Frankfurt, Germany.ORCID 0000-0002-9528-8822
Matthias KleinInstitute of Immunology, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany.
Christian MichelDepartment of Hematology, Medical Oncology, & Pneumology, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany.
Markus P RadsakDepartment of Hematology, Medical Oncology, & Pneumology, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany.
Sebastian RosigkeitCell Biology Unit, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany.
Peter GrimmingerDepartment of General, Visceral- and Transplant Surgery, University Medical Center, Mainz, Germany.
Hansjörg SchildInstitute of Immunology, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany.
Krishnaraj RajalingamCell Biology Unit, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany.ORCID 0000-0002-4175-9633
Johannes Gutenberg University Mainz · DEGoethe University Frankfurt · DEUniversity of Freiburg · DEWilkes University · US

Funding

Deutsche Forschungsgemeinschaft CRC1292Deutsche Forschungsgemeinschaft RA1739/4-1Deutsche Forschungsgemeinschaft RA1739/4-2Else Kröner-Fresenius-Stiftung SUNMAPKMerck KGaA ERK-KR
6 · The paper itself

Abstract

ERK3 is a ubiquitously expressed member of the atypical mitogen activated protein kinases (MAPKs) and the physiological significance of its short half-life remains unclear. By employing gastrointestinal 3D organoids, we detect that ERK3 protein levels steadily decrease during epithelial differentiation. ERK3 is not required for 3D growth of human gastric epithelium. However, ERK3 is stabilized and activated in tumorigenic cells, but deteriorates over time in primary cells in response to lipopolysaccharide (LPS). ERK3 is necessary for production of several cellular factors including interleukin-8 (IL-8), in both, normal and tumorigenic cells. Particularly, ERK3 is critical for AP-1 signaling through its interaction and regulation of c-Jun protein. The secretome of ERK3-deficient cells is defective in chemotaxis of neutrophils and monocytes both in vitro and in vivo. Further, knockdown of ERK3 reduces metastatic potential of invasive breast cancer cells. We unveil an ERK3-mediated regulation of IL-8 and epithelial secretome for chemotaxis.

Indexed as

AnimalsCell LineChemotaxis, LeukocyteGene Expression RegulationHeterograftsHumansInterleukin-8MiceMitogen-Activated Protein Kinase 6CXCL8 protein, humanInterleukin-8Mitogen-Activated Protein Kinase 6cell biologychemotaxisERK3gastrointestinal organoidshumanIL-8MAPKmetastasismousesecretomesignal transduction

Identifiers

PMID32314963
PMCPMC7192585
OpenAlexW3016365362

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.