Evidence map›Paper›PMID 26446844›Full record

ArticleMolecular biology of the cell2015

In vivo quantitative analysis of Talin turnover in response to force.

Guðlaug Katrín Hákonardóttir, Pablo López-Ceballos, Alejandra Donají Herrera-Reyes, Raibatak Das, Daniel Coombs, Guy Tanentzapf

Open access · greenAbstract read
In one paragraph

Article in Molecular biology of the cell, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

12 citing papers in PubMed, 25 citations in OpenAlex.

  1. Review
  2. Review
  3. Allosteric activation of vinculin by talin.Nature communications · 2023
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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

6 authors at 2 institutions in 2 countries.

Guðlaug Katrín HákonardóttirDepartment of Cellular and Physiological Sciences, Life Science Institute, University of British Columbia, Vancouver, BC V6T 1Z3, Canada.
Pablo López-CeballosDepartment of Cellular and Physiological Sciences, Life Science Institute, University of British Columbia, Vancouver, BC V6T 1Z3, Canada.
Alejandra Donají Herrera-ReyesDepartment of Mathematics and Institute of Applied Mathematics, University of British Columbia, Vancouver, BC V6T 1Z2, Canada.
Raibatak DasDepartment of Integrative Biology, University of Colorado Denver, Denver, CO 80204.
Daniel CoombsDepartment of Mathematics and Institute of Applied Mathematics, University of British Columbia, Vancouver, BC V6T 1Z2, Canada.
Guy TanentzapfDepartment of Cellular and Physiological Sciences, Life Science Institute, University of British Columbia, Vancouver, BC V6T 1Z3, Canada tanentz@mail.ubc.ca.
University of British Columbia · CAUniversity of Colorado Denver · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cell adhesion to the extracellular matrix (ECM) allows cells to form and maintain three-dimensional tissue architecture. Cell-ECM adhesions are stabilized upon exposure to mechanical force. In this study, we used quantitative imaging and mathematical modeling to gain mechanistic insight into how integrin-based adhesions respond to increased and decreased mechanical forces. A critical means of regulating integrin-based adhesion is provided by modulating the turnover of integrin and its adhesion complex (integrin adhesion complex [IAC]). The turnover of the IAC component Talin, a known mechanosensor, was analyzed using fluorescence recovery after photobleaching. Experiments were carried out in live, intact flies in genetic backgrounds that increased or decreased the force applied on sites of adhesion. This analysis showed that when force is elevated, the rate of assembly of new adhesions increases such that cell-ECM adhesion is stabilized. Moreover, under conditions of decreased force, the overall rate of turnover, but not the proportion of adhesion complex components undergoing turnover, increases. Using point mutations, we identify the key functional domains of Talin that mediate its response to force. Finally, by fitting a mathematical model to the data, we uncover the mechanisms that mediate the stabilization of ECM-based adhesion during development.

Indexed as

AnimalsCell AdhesionCell-Matrix JunctionsCell MembraneDrosophilaExtracellular MatrixFocal AdhesionsIntegrinsMaleModels, BiologicalStress, PhysiologicalTalinIntegrinsTalin

Identifiers

PMID26446844
PMCPMC4710244
OpenAlexW2302921696

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.