Evidence map›Paper›PMID 23336027›Full record

ArticleCommunicative & integrative biology2012

Mechano-sensing by actin filaments and focal adhesion proteins.

Kimihide Hayakawa, Hitoshi Tatsumi, Masahiro Sokabe

Open access · goldAbstract read
In one paragraph

Article in Communicative & integrative biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.3field-weighted citation impact, top 24% 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

17 citing papers in PubMed, 44 citations in OpenAlex.

  1. Article
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  16. Hydrogels preserve native phenotypes of valvular fibroblasts through an elasticity-regulated PI3K/AKT pathway.Proceedings of the National Academy of Sciences of the United States of America · 2013
    Article
  17. Article
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

3 authors at 1 institution in 1 country.

Kimihide HayakawaFIRST Research Center for Innovative Nanobiodevice; Nagoya University; Nagoya, Japan.
Hitoshi Tatsumi
Masahiro Sokabe
Nagoya University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mechanosensitive ion channels have long been the only established molecular class of cell mechanosensors with known molecular entities. However, recent advances in the state-of-the-art techniques, including single-molecule manipulation and imaging, have enabled an investigation of non-channel type cell mechanosensors and the underlying biophysical mechanisms of their activation. To date, two focal adhesion proteins, talin and p130Cas, have been postulated to act as putative mechanosensors, acting through mechano-induced unfolding of their particular soft domain(s) susceptible to phosphorylation. More recently, the actin filament has been demonstrated to act as a mechanosensor in the presence of the soluble actin-severing protein, cofilin. The cofilin severing activity negatively depends on the tension in the actin filament through tension-dependent binding/unbinding of cofilin to/from the actin filament. As a result, relaxed actin filaments are severed, while tensed ones are either not severed or severed after a long delay. Here we review the latest progress in the mechanosensing by non-channel type proteins and discuss the possible physiological roles of the mechanosensing performed by actin filaments in the course of cell migration.

Indexed as

actinsADF/Cofilinfocal adhesionsmechanosensingstress fiberstension

Identifiers

PMID23336027
PMCPMC3541324
OpenAlexW1985636946

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.