Evidence map›Paper›PMID 30612939›Full record

ArticleDevelopmental cell2019

The Atypical MAP Kinase ErkB Transmits Distinct Chemotactic Signals through a Core Signaling Module.

John M E Nichols, Peggy Paschke, Sew Peak-Chew, Thomas D Williams, Luke Tweedy, Mark Skehel, Elaine Stephens, Jonathan R Chubb, Robert R Kay

Open access · hybridAbstract read
In one paragraph

Article in Developmental cell, 2019. 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 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, 38 citations in OpenAlex.

  1. Article
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  9. Article
  10. The MAPK/ERK channel capacity exceeds 6 bit/hour.PLoS computational biology · 2023
    Article
  11. Heliyon · 2023
    Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 4 institutions in 2 countries.

John M E NicholsCell Biology Division, MRC Laboratory of Molecular Biology, Francis Crick Avenue, Cambridge CB2 0QH, UK; MRC Laboratory for Molecular Cell Biology, University College London, Gower St., London WC1E 6BT, UK. Electronic address: j.nichols@ucl.ac.uk.
Peggy PaschkeCell Biology Division, MRC Laboratory of Molecular Biology, Francis Crick Avenue, Cambridge CB2 0QH, UK; Cancer Research UK (CRUK) Beatson Institute, University of Glasgow, Bearsden, Glasgow G61 1BD, UK. Electronic address: ppaschke@mrc-lmb.cam.ac.uk.
Sew Peak-ChewCell Biology Division, MRC Laboratory of Molecular Biology, Francis Crick Avenue, Cambridge CB2 0QH, UK.
Thomas D WilliamsCell Biology Division, MRC Laboratory of Molecular Biology, Francis Crick Avenue, Cambridge CB2 0QH, UK.
Luke TweedyCancer Research UK (CRUK) Beatson Institute, University of Glasgow, Bearsden, Glasgow G61 1BD, UK.
Mark SkehelCell Biology Division, MRC Laboratory of Molecular Biology, Francis Crick Avenue, Cambridge CB2 0QH, UK.
Elaine StephensCell Biology Division, MRC Laboratory of Molecular Biology, Francis Crick Avenue, Cambridge CB2 0QH, UK; Pfizer Inc, 1 Burtt Road, Andover, MA 01810, USA.
Jonathan R ChubbMRC Laboratory for Molecular Cell Biology and Department of Cell and Developmental Biology, University College London, Gower St., London WC1E 6BT, UK.
Robert R KayCell Biology Division, MRC Laboratory of Molecular Biology, Francis Crick Avenue, Cambridge CB2 0QH, UK. Electronic address: rrk@mrc-lmb.cam.ac.uk.
MRC Laboratory of Molecular Biology · GBUniversity College London · GBCancer Research UK Scotland Institute · GBUniversity of Glasgow · GB

Funding

Medical Research Council MC_U105115237Medical Research Council MC_U105184326Medical Research Council MC_U12266BWellcome TrustWellcome Trust 202867/Z/16/Z
6 · The paper itself

Abstract

Signaling from chemoattractant receptors activates the cytoskeleton of crawling cells for chemotaxis. We show using phosphoproteomics that different chemoattractants cause phosphorylation of the same core set of around 80 proteins in Dictyostelium cells. Strikingly, the majority of these are phosphorylated at an [S/T]PR motif by the atypical MAP kinase ErkB. Unlike most chemotactic responses, ErkB phosphorylations are persistent and do not adapt to sustained stimulation with chemoattractant. ErkB integrates dynamic autophosphorylation with chemotactic signaling through G-protein-coupled receptors. Downstream, our phosphoproteomics data define a broad panel of regulators of chemotaxis. Surprisingly, targets are almost exclusively other signaling proteins, rather than cytoskeletal components, revealing ErkB as a regulator of regulators rather than acting directly on the motility machinery. ErkB null cells migrate slowly and orientate poorly over broad dynamic ranges of chemoattractant. Our data indicate a central role for ErkB and its substrates in directing chemotaxis.

Indexed as

AnimalsChemotactic FactorsChemotaxisCyclic AMPCytoskeletonDictyosteliumMitogen-Activated Protein KinasesPhosphorylationReceptors, G-Protein-CoupledSignal TransductionChemotactic FactorsCyclic AMPMitogen-Activated Protein KinasesReceptors, G-Protein-CoupledchemotaxisDictyostelium discoideumMAPK signalingphosphoproteomicsprotein kinaseprotein phosphorylationsignal transduction

Identifiers

PMID30612939
PMCPMC6397043
OpenAlexW2907359184

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.