Evidence map›Paper›PMID 15138291›Full record

ArticleThe Journal of cell biology2004

Vinculin modulation of paxillin-FAK interactions regulates ERK to control survival and motility.

M Cecilia Subauste, Olivier Pertz, Eileen D Adamson, Christopher E Turner, Sachiko Junger, Klaus M Hahn

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 117 papers.

0numbers the graph read from it
0cells of the map it votes in
117citing papers in PubMed
5.8field-weighted citation impact, top 3% 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

117 citing papers in PubMed, 267 citations in OpenAlex.

  1. Article
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  5. Cancer chemoprevention: signaling pathways and strategic approaches.Signal transduction and targeted therapy · 2025
    Review
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  18. Review
  19. Paxillin Is Required for Proper Spinal Motor Axon Growth into the Limb.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
    Article
  20. Article

57 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

6 authors at 3 institutions in 1 country.

M Cecilia SubausteDepartment of Cell Biology, The Scripps Research Institute, La Jolla, CA 92037, USA.
Olivier Pertz
Eileen D Adamson
Christopher E Turner
Sachiko Junger
Klaus M Hahn
Scripps Research Institute · USSanford Burnham Prebys Medical Discovery Institute · USSUNY Upstate Medical University · US

Funding

STRUCTURE AND FUNCTION OF PAXILLINR01GM047607 · NIGMS · UPSTATE MEDICAL UNIVERSITY · PI TURNER, CHRISTOPHER E · 1996 to 2017
$5.5M
ROLES OF EGR AND FOS IN DEVELOPMENT AND CANCERR01CA067888 · NCI · BURNHAM INSTITUTE FOR MEDICAL RESEARCH · PI ADAMSON, EILEEN D · 1995 to 2004
$1.8M
RHO FAMILY GTPASES AND APOPTOTIC SIGNALINGR01AG015430 · NIA · UNIVERSITY OF NORTH CAROLINA CHAPEL HILL · PI HAHN, KLAUS MICHAEL · 1997 to 2004
$1.6M
RHO GTPASE FAMILY IN INDUCTION OF APOPTOSISK08AI001684 · NIAID · SCRIPPS RESEARCH INSTITUTE · PI SUBAUSTE, MARIA CECILIA · 1999 to 2002
$263k
STRUCTURE AND FUNCTION OF PAXILLINR29GM047607 · NIGMS · UPSTATE MEDICAL UNIVERSITY · PI TURNER, CHRISTOPHER E · 1991 to 1995
–
NCI NIH HHS CA 67888NCI NIH HHS R01 CA067888NIAID NIH HHS AI 01684-02NIA NIH HHS AG 15430NIA NIH HHS R01 AG015430NIGMS NIH HHS GM 47607NIGMS NIH HHS R01 GM047607
6 · The paper itself

Abstract

Cells lacking vinculin are highly metastatic and motile. The reasons for this finding have remained unclear. Both enhanced survival and motility are critical to metastasis. Here, we show that vinculin null (vin-/-) cells and cells expressing a vinculin Y822F mutant have increased survival due to up-regulated activity of extracellular signal-regulated kinase (ERK). This increase is shown to result from vinculin's modulation of paxillin-FAK interactions. A vinculin fragment (amino acids 811-1066) containing the paxillin binding site restored apoptosis and suppressed ERK activity in vin-/- cells. Both vinY822F and vin-/- cells exhibit increased interaction between paxillin and focal adhesion kinase (FAK) and increased paxillin and FAK phosphorylation. Transfection with paxillin Y31FY118F dominant-negative mutant in these cells inhibits ERK activation and restores apoptosis. The enhanced motility of vin-/- and vinY822F cells is also shown to be due to a similar mechanism. Thus, vinculin regulates survival and motility via ERK by controlling the accessibility of paxillin for FAK interaction.

Indexed as

AnimalsApoptosisBinding SitesCell AdhesionCell MovementCell SurvivalCytoskeletal ProteinsFocal Adhesion Kinase 1Focal Adhesion Protein-Tyrosine KinasesMiceMitogen-Activated Protein KinasesMutationNeoplasm MetastasisNeoplastic Stem CellsPaxillinPeptide FragmentsCytoskeletal ProteinsFocal Adhesion Kinase 1Focal Adhesion Protein-Tyrosine KinasesMitogen-Activated Protein KinasesPaxillinPeptide FragmentsPhosphoproteinsProtein-Tyrosine KinasesPtk2 protein, mousePxn protein, mouseVinculin

Identifiers

PMID15138291
PMCPMC2172187
OpenAlexW2100491916

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.