Evidence map›Paper›PMID 19171760›Full record

ArticleThe Journal of cell biology2009

Integrin alpha3beta1-dependent beta-catenin phosphorylation links epithelial Smad signaling to cell contacts.

Young Kim, Matthias C Kugler, Ying Wei, Kevin K Kim, Xiaopeng Li, Alexis N Brumwell, Harold A Chapman

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 papers.

0numbers the graph read from it
0cells of the map it votes in
90citing papers in PubMed
8.5field-weighted citation impact, top 1% 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

90 citing papers in PubMed, 159 citations in OpenAlex.

  1. Article
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  7. Myofibroblast specific targeting approaches to improve fibrosis treatment.Chemical communications (Cambridge, England) · 2022
    Review
  8. Article
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  12. Pathophysiology of Lung Disease and Wound Repair in Cystic Fibrosis.Pathophysiology : the official journal of the International Society for Pathophysiology · 2021
    Review
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  15. Article
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  20. Article

30 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

7 authors at 1 institution in 1 country.

Young KimPulmonary and Critical Care Division, Department of Medicine, and Cardiovascular Research Institute, University of California, San Francisco, San Francisco, CA 94143, USA.
Matthias C Kugler
Ying Wei
Kevin K Kim
Xiaopeng Li
Alexis N Brumwell
Harold A Chapman
University of California, San Francisco · US

Funding

MUTIDISCIPLINARY TRAINING PROGRAM IN LUNG DISEASEST32HL007185 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI David J Erle, LAURENCE HUANG · 1985 to 2026
$24.6M
REGULATION OF INTEGRIN FUNCTIONR01HL044712 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI CHAPMAN, HAROLD A · 1991 to 2014
$4.8M
Alpha3Beta Integrin Function in Epithelial-Mesenchymal Transition and FibrosisK08HL085290 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI KIM, KEVIN KEEWOUN · 2007 to 2011
$625k
NHLBI NIH HHS K08 HL 085290NHLBI NIH HHS K08 HL085290NHLBI NIH HHS R01 HL044712NHLBI NIH HHS R01 HL44712NHLBI NIH HHS T32 HL 007185NHLBI NIH HHS T32 HL007185
6 · The paper itself

Abstract

Injury-initiated epithelial to mesenchymal transition (EMT) depends on contextual signals from the extracellular matrix, suggesting a role for integrin signaling. Primary epithelial cells deficient in their prominent laminin receptor, alpha3beta1, were found to have a markedly blunted EMT response to TGF-beta1. A mechanism for this defect was explored in alpha3-null cells reconstituted with wild-type (wt) alpha3 or point mutants unable to engage laminin 5 (G163A) or epithelial cadherin (E-cadherin; H245A). After TGF-beta1 stimulation, wt epithelial cells but not cells expressing the H245A mutant internalize complexes of E-cadherin and TGF-beta1 receptors, generate phospho-Smad2 (p-Smad2)-pY654-beta-catenin complexes, and up-regulate mesenchymal target genes. Although Smad2 phosphorylation is normal, p-Smad2-pY654-beta-catenin complexes do not form in the absence of alpha3 or when alpha3beta1 is mainly engaged on laminin 5 or E-cadherin in adherens junctions, leading to attenuated EMT. These findings demonstrate that alpha3beta1 coordinates cross talk between beta-catenin and Smad signaling pathways as a function of extracellular contact cues and thereby regulates responses to TGF-beta1 activation.

Indexed as

Animalsbeta CateninCell AdhesionEpithelial CellsEpitheliumFluorescent Antibody TechniqueIntegrin alpha3beta1MiceMice, TransgenicPhosphorylationSignal TransductionSmad ProteinsTransforming Growth Factor beta1beta CateninIntegrin alpha3beta1Smad ProteinsTransforming Growth Factor beta1

Identifiers

PMID19171760
PMCPMC2654298
OpenAlexW2108119086

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.