Evidence map›Paper›PMID 25990957›Full record

ArticleScience signaling2015

ERK reinforces actin polymerization to power persistent edge protrusion during motility.

Michelle C Mendoza, Marco Vilela, Jesus E Juarez, John Blenis, Gaudenz Danuser

Open access · greenAbstract read
In one paragraph

Article in Science signaling, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed
3.8field-weighted citation impact, top 7% 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

66 citing papers in PubMed, 100 citations in OpenAlex.

  1. Article
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  4. ERK builds a population of short-lived nascent adhesions that produce persistent edge protrusion and cell migration.Proceedings of the National Academy of Sciences of the United States of America · 2026
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  5. Allosteric Biosensors Unravel GTPase-Effector Feedback.bioRxiv : the preprint server for biology · 2026
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  15. pERK transition-induced directional mode switching promotes epithelial tumor cell migration.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
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  18. [Role and mechanism of cysteine and glycine-rich protein 2 in the malignant progression of neuroblastoma].Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences · 2024
    Article
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6 more citing papers are in PubMed but not listed here.

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

5 authors at 1 institution in 1 country.

Michelle C MendozaDepartment of Cell Biology, Harvard Medical School, Boston, MA 02115, USA. michelle.mendoza@ucsf.edu gaudenz.danuser@utsouthwestern.edu.
Marco VilelaDepartment of Cell Biology, Harvard Medical School, Boston, MA 02115, USA.
Jesus E JuarezDepartments of Cell and Tissue Biology and Pathology, University of California, San Francisco, 513 Parnassus Avenue, San Francisco, CA 94143, USA.
John BlenisDepartment of Cell Biology, Harvard Medical School, Boston, MA 02115, USA.
Gaudenz DanuserDepartment of Cell Biology, Harvard Medical School, Boston, MA 02115, USA. michelle.mendoza@ucsf.edu gaudenz.danuser@utsouthwestern.edu.
Harvard University · US

Funding

ONCOGENIC REGULATION OF S6 PROTEIN KINASE &CELL GROWTHR01CA046595 · NCI · WEILL MEDICAL COLL OF CORNELL UNIV · PI JOHN BLENIS · 1988 to 2026
$10.6M
The Mechanics of Actin-mediated Cell ProtrusionR01GM071868 · NIGMS · UT SOUTHWESTERN MEDICAL CENTER · PI DANUSER, GAUDENZ · 2007 to 2020
$2.9M
Quantitative Fluorescent Speckle MicroscopyU01GM067230 · NIGMS · SCRIPPS RESEARCH INSTITUTE, THE · PI DANUSER, GAUDENZ · 2008 to 2011
$1.7M
Regulation of Cell Motility by the Oncogenic ERK-MAPK PathwayK01CA168850 · NCI · UNIVERSITY OF UTAH · PI MENDOZA, MICHELLE CHRISTINE · 2012 to 2016
$690k
Signaling network reconstruction from biosensor image fluctuationsF32GM103278 · NIGMS · HARVARD MEDICAL SCHOOL · PI VILELA, MARCO ANTONIO · 2012 to 2014
$80k
NCI NIH HHS K01 CA168850NCI NIH HHS R01 CA046595NCI NIH HHS R01CA046595NIGMS NIH HHS F32 GM103278NIGMS NIH HHS R01 GM071868NIGMS NIH HHS U01 GM067230NIGMS NIH HHS U01 GM068230
6 · The paper itself

Abstract

Cells move through perpetual protrusion and retraction cycles at the leading edge. These cycles are coordinated with substrate adhesion and retraction of the cell rear. We tracked spatial and temporal fluctuations in the molecular activities of individual moving cells to elucidate how extracellular signal-regulated kinase (ERK) signaling controlled the dynamics of protrusion and retraction cycles. ERK is activated by many cell surface receptors, and we found that ERK signaling specifically reinforced cellular protrusions so that they translated into rapid, sustained forward motion of the leading edge. Using quantitative fluorescent speckle microscopy and cross-correlation analysis, we showed that ERK controlled the rate and timing of actin polymerization by promoting the recruitment of the actin nucleator Arp2/3 to the leading edge. These findings support a model in which surges in ERK activity induced by extracellular cues enhance Arp2/3-mediated actin polymerization to generate protrusion power phases with enough force to counteract increasing membrane tension and to promote sustained motility.

Indexed as

Models, BiologicalActin-Related Protein 2-3 ComplexActinsBenzimidazolesBiomechanical PhenomenaCell Line, TumorCell MovementCell Surface ExtensionsFluorescent Antibody TechniqueHumansImage Processing, Computer-AssistedMAP Kinase Kinase 1MAP Kinase Kinase 2MAP Kinase Signaling SystemMicroscopy, FluorescencePolymerizationActin-Related Protein 2-3 ComplexActinsAZD 6244BenzimidazolesMAP2K2 protein, humanMAP Kinase Kinase 1MAP Kinase Kinase 2

Identifiers

PMID25990957
PMCPMC4830495
OpenAlexW1905742426

What OpenQuestion holds

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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.