Evidence map›Paper›PMID 28768826›Full record

ArticleMolecular biology of the cell2017

Mechanical signals activate p38 MAPK pathway-dependent reinforcement of actin via mechanosensitive HspB1.

Laura Hoffman, Christopher C Jensen, Masaaki Yoshigi, Mary Beckerle

Abstract read
In one paragraph

Article in Molecular biology of the cell, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed
3.4field-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

63 citing papers in PubMed, 93 citations in OpenAlex.

  1. Review
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  10. Acetylation and Deacetylation of Cytoskeleton-Associated Proteins.Results and problems in cell differentiation · 2025
    Review
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3 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

4 authors at 1 institution in 1 country.

Laura HoffmanHuntsman Cancer Institute, University of Utah, Salt Lake City, UT 84112.
Christopher C JensenHuntsman Cancer Institute, University of Utah, Salt Lake City, UT 84112.
Masaaki YoshigiHuntsman Cancer Institute, University of Utah, Salt Lake City, UT 84112.
Mary BeckerleHuntsman Cancer Institute, University of Utah, Salt Lake City, UT 84112 Mary.beckerle@hci.utah.edu.
University of Utah · US

Funding

UTAH REGIONAL CANCER CENTERP30CA042014 · NCI · UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH · PI Jared P Rutter · 1986 to 2026
$72.6M
Proteomics CoreU54DK110858 · NIDDK · UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH · PI Anna E Beaudin, JAMES Eric COX · 2016 to 2026
$8.6M
Structure and function of stress fibers and cell adhesion sitesR01GM050877 · NIGMS · UNIVERSITY OF UTAH · PI BECKERLE, MARY C. · 1994 to 2020
$7.8M
NCRR Confocal ProposalS10RR024761 · NCRR · UNIVERSITY OF UTAH · PI RODESCH, CHRISTOPHER K · 2008 to 2008
$475k
NCI NIH HHS P30 CA042014NCRR NIH HHS S10 RR024761NIDDK NIH HHS U54 DK110858NIGMS NIH HHS R01 GM050877
6 · The paper itself

Abstract

Despite the importance of a cell's ability to sense and respond to mechanical force, the molecular mechanisms by which physical cues are converted to cell-instructive chemical information to influence cell behaviors remain to be elucidated. Exposure of cultured fibroblasts to uniaxial cyclic stretch results in an actin stress fiber reinforcement response that stabilizes the actin cytoskeleton. p38 MAPK signaling is activated in response to stretch, and inhibition of p38 MAPK abrogates stretch-induced cytoskeletal reorganization. Here we show that the small heat shock protein HspB1 (hsp25/27) is phosphorylated in stretch-stimulated mouse fibroblasts via a p38 MAPK-dependent mechanism. Phosphorylated HspB1 is recruited to the actin cytoskeleton, displaying prominent accumulation on actin "comet tails" that emanate from focal adhesions in stretch-stimulated cells. Site-directed mutagenesis to block HspB1 phosphorylation inhibits the protein's cytoskeletal recruitment in response to mechanical stimulation. HspB1-null cells, generated by CRISPR/Cas9 nuclease genome editing, display an abrogated stretch-stimulated actin reinforcement response and increased cell migration. HspB1 is recruited to sites of increased traction force in cells geometrically constrained on micropatterned substrates. Our findings elucidate a molecular pathway by which a mechanical signal is transduced via activation of p38 MAPK to influence actin remodeling and cell migration via a zyxin-independent process.

Indexed as

MAP Kinase Signaling SystemActin CytoskeletonActinsAnimalsCell MovementCells, CulturedCytoskeletal ProteinsCytoskeletonFibroblastsFocal AdhesionsHeat-Shock ProteinsMechanical PhenomenaMiceMolecular ChaperonesNeoplasm Proteinsp38 Mitogen-Activated Protein KinasesActinsCytoskeletal ProteinsHeat-Shock ProteinsHsbp1 protein, mouseMolecular ChaperonesNeoplasm Proteinsp38 Mitogen-Activated Protein KinasesZyxinZyx protein, mouse

Identifiers

PMID28768826
PMCPMC5620374
OpenAlexW2741543122

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.