Evidence map›Paper›PMID 22441983›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2012

LNK (SH2B3) is a key regulator of integrin signaling in endothelial cells and targets α-parvin to control cell adhesion and migration.

Julie Devallière, Mathias Chatelais, Juliette Fitau, Nathalie Gérard, Philippe Hulin, Laura Velazquez, Christopher E Turner, Béatrice Charreau

Abstract read
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 3 pooled it
4.2field-weighted citation impact, top 6% 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

28 citing papers in PubMed, 3 syntheses or guidelines pooled it, 47 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Overlap between common genetic polymorphisms underpinning kidney traits and cardiovascular disease phenotypes: the CKDGen consortium.American journal of kidney diseases : the official journal of the National Kidney Foundation · 2013
    Pooled it
  4. Lnk Governs chemokine-directed trafficking of CD8Molecular therapy. Oncology · 2026
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  19. Bortezomib, C1-inhibitor and plasma exchange do not prolong the survival of multi-transgenic GalT-KO pig kidney xenografts in baboons.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2015
    Article
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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

8 authors at 4 institutions in 2 countries.

Julie DevallièreInstitut National de la Santé et de la Recherche Médicale (INSERM), Unité Mixte de Recherche (UMR) 643, Nantes, France.
Mathias Chatelais
Juliette Fitau
Nathalie Gérard
Philippe Hulin
Laura Velazquez
Christopher E Turner
Béatrice Charreau
Inserm · FRCentre Hospitalier Universitaire de Nantes · FRNantes Université · FRSUNY Upstate Medical University · US

Funding

ILK-Actopaxin Interactions in Cell SignalingR01HL070244 · NHLBI · UPSTATE MEDICAL UNIVERSITY · PI TURNER, CHRISTOPHER E · 2002 to 2010
$3.0M
NHLBI NIH HHS R01 HL070244NHLBI NIH HHS R01-HL-070244
6 · The paper itself

Abstract

Focal adhesion (FA) formation and disassembly play an essential role in adherence and migration of endothelial cells. These processes are highly regulated and involve various signaling molecules that are not yet completely identified. Lnk [Src homology 2-B3 (SH2B3)] belongs to a family of SH2-containing proteins with important adaptor functions. In this study, we showed that Lnk distribution follows that of vinculin, localizing Lnk in FAs. Inhibition of Lnk by RNA interference resulted in decreased spreading, whereas sustained expression dramatically increases the number of focal and cell-matrix adhesions. We demonstrated that Lnk expression impairs FA turnover and cell migration and regulates β1-integrin-mediated signaling via Akt and GSK3β phosphorylation. Moreover, the α-parvin protein was identified as one of the molecular targets of Lnk responsible for impaired FA dynamics and cell migration. Finally, we established the ILK protein as a new molecular partner for Lnk and proposed a model in which Lnk regulates α-parvin expression through its interaction with ILK. Collectively, our results underline the adaptor Lnk as a novel and effective key regulator of integrin-mediated signaling controlling endothelial cell adhesion and migration.

Indexed as

Adaptor Proteins, Signal TransducingCalponinsCell AdhesionCell-Matrix JunctionsCell MovementFocal AdhesionsHumansHuman Umbilical Vein Endothelial CellsIntegrin beta1Intracellular Signaling Peptides and ProteinsMicrofilament ProteinsProteinsProtein Serine-Threonine KinasesProto-Oncogene Proteins c-aktScaffold Protein ILKSignal TransductionAdaptor Proteins, Signal TransducingCalponinsIntegrin beta1Intracellular Signaling Peptides and ProteinsMicrofilament ProteinsPARVA protein, humanProteinsProtein Serine-Threonine KinasesProto-Oncogene Proteins c-aktScaffold Protein ILKSH2B3 protein, human

Identifiers

PMID22441983
PMCPMC3360145
OpenAlexW1982640569

What Socratic holds

Textmetadata
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 Socratic graph.