Evidence map›Paper›PMID 21900245›Full record

ArticleThe Journal of biological chemistry2011

Paxillin enables attachment-independent tyrosine phosphorylation of focal adhesion kinase and transformation by RAS.

Ramon Wade, Nicole Brimer, Charles Lyons, Scott Vande Pol

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.1field-weighted citation impact, top 27% 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

14 citing papers in PubMed, 15 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Paxillin: a crossroad in pathological cell migration.Journal of hematology & oncology · 2017
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. The role of FAK in tumor metabolism and therapy.Pharmacology & therapeutics · 2014
    Review
  12. mTORC2 regulates mechanically induced cytoskeletal reorganization and lineage selection in marrow-derived mesenchymal stem cells.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2014
    Article
  13. Article
  14. 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

4 authors at 1 institution in 1 country.

Ramon WadeDepartment of Pathology, University of Virginia, Charlottesville, Virginia 22908.
Nicole BrimerDepartment of Pathology, University of Virginia, Charlottesville, Virginia 22908.
Charles LyonsDepartment of Pathology, University of Virginia, Charlottesville, Virginia 22908.
Scott Vande PolDepartment of Pathology, University of Virginia, Charlottesville, Virginia 22908. Electronic address: vandepol@virginia.edu.
University of Virginia · US

Funding

Papillomavirus E6 Structural ConsortiumR01CA134737 · NCI · UNIVERSITY OF VIRGINIA · PI VANDE POL, SCOTT BRIAN · 2010 to 2019
$4.2M
Papillomavirus TransformationR01CA069292 · NCI · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI VANDE POL, SCOTT BRIAN · 2002 to 2006
$1.4M
E6 Interaction with Cellular PDZ ProteinsR01CA120352 · NCI · UNIVERSITY OF VIRGINIA · PI VANDE POL, SCOTT BRIAN · 2007 to 2010
$1.2M
PAPILLOMAVIRUS TRANSFORMATIONR29CA069292 · NCI · CASE WESTERN RESERVE UNIVERSITY · PI VANDE POL, SCOTT B · 1996 to 2000
$35k
NCI NIH HHS CA120352NCI NIH HHS CA-69292NCI NIH HHS R01 CA069292NCI NIH HHS R01 CA120352NCI NIH HHS R01 CA134737NCI NIH HHS R29 CA069292
6 · The paper itself

Abstract

Paxillin and HIC5 are closely related adapter proteins that regulate cell migration and are tyrosine-phosphorylated by focal adhesion kinase (FAK). Paxillin, HIC5, and FAK tyrosine phosphorylation increase upon cell attachment and decrease upon detachment from extracellular matrix. Unexpectedly, we found that although FAK tyrosine phosphorylation in attached cells did not require paxillin, in detached fibroblasts there was remaining FAK tyrosine phosphorylation that required expression of paxillin and was not supported by HIC5. The support of attachment-independent FAK tyrosine phosphorylation required the paxillin LIM domains and suggested that paxillin might facilitate oncogenic transformation. Paxillin but not HIC5 augmented anchorage-independent cell proliferation induced by RAS. Both anchorage-independent FAK tyrosine phosphorylation and RAS-induced colony formation required multiple docking sites on paxillin, including LD4 (docking sites for FAK-Src and GIT1/2-PIX-NCK-PAK complex), LD5, and all four carboxyl-terminal LIM domains (that bind tubulin and PTP-PEST). Analysis using paxillin mutants dissociated domains of paxillin that are required for regulation of cell migration from domains that are required for anchorage-independent cell proliferation and demonstrated essential functions of the paxillin LIM domains that are not found in HIC5 LIM domains. These results highlight the role of paxillin in facilitating attachment-independent signal transduction implicated in cancer.

Indexed as

ActinsAnimalsCell AdhesionCell ProliferationCytoskeletal ProteinsCytoskeletonDNA-Binding ProteinsEnzyme ActivationFibroblastsFocal Adhesion Protein-Tyrosine KinasesHumansIntracellular Signaling Peptides and ProteinsLIM Domain ProteinsMiceMutationPaxillinActinsCytoskeletal ProteinsDNA-Binding ProteinsFocal Adhesion Protein-Tyrosine KinasesIntracellular Signaling Peptides and ProteinsLIM Domain ProteinsPaxillinras ProteinsTGFB1I1 protein, humanTgfb1i1 protein, mouseTyrosine

Identifiers

PMID21900245
PMCPMC3207406
OpenAlexW2016529720

What OpenQuestion 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 OpenQuestion graph.