Evidence map›Paper›PMID 23295182›Full record

ArticleThe Journal of biological chemistry2013

ARAP2 signals through Arf6 and Rac1 to control focal adhesion morphology.

Pei-Wen Chen, Xiaoying Jian, Hye-Young Yoon, Paul A Randazzo

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.8field-weighted citation impact, top 18% 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

22 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. Article
  3. ACancers · 2021
    Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Arf GAPs as Regulators of the Actin Cytoskeleton-An Update.International journal of molecular sciences · 2019
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. A genome-wide identified risk variant for PTSD is a methylation quantitative trait locus and confers decreased cortical activation to fearful faces.American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics · 2015
    Article
  18. Inhibition of Cytohesins Protects against Genetic Models of Motor Neuron Disease.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015
    Article
  19. Article
  20. 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.

Pei-Wen ChenLaboratory of Cellular and Molecular Biology, NCI, National Institutes of Health, Bethesda, Maryland 20892, USA.
Xiaoying Jian
Hye-Young Yoon
Paul A Randazzo
National Institutes of Health · US

Funding

Regulation of ADP-ribosylation factorZIABC007365 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI RANDAZZO, PAUL A · 2009 to 2025
$27.9M
REGULATION OF ADP-RIBOSYLATION FACTORZ01BC007365 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI RANDAZZO, PAUL A · 1996 to 2008
$3.3M
Intramural NIH HHS Z01 BC007365
6 · The paper itself

Abstract

Focal adhesions (FAs) are dynamic structures that connect the actin cytoskeleton with the extracellular matrix. At least six ADP-ribosylation factor (Arf) GTPase-activating proteins (GAPs), including ARAP2 (an Arf6 GAP), are implicated in regulation of FAs but the mechanisms for most are not well defined. Although Rac1 has been reported to function downstream of Arf6 to control membrane ruffling and cell migration, this pathway has not been directly examined as a regulator of FAs. Here we test the hypothesis that ARAP2 promotes the growth of FAs by converting Arf6·GTP to Arf6·GDP thereby preventing the activation of the Rho family GTP-binding protein Rac1. Reduced expression of ARAP2 decreased the number and size of FAs in cells and increased cellular Arf6·GTP and Rac1·GTP levels. Overexpression of ARAP2 had the opposite effects. The effects of ARAP2 on FAs and Rac1 were dependent on a functional ArfGAP domain. Constitutively active Arf6 affected FAs in the same way as did reduced ARAP2 expression and dominant negative mutants of Arf6 and Rac1 reversed the effect of reduced ARAP2 expression. However, neither dominant negative Arf6 nor Rac1 had the same effect as ARAP2 overexpression. We conclude that changes in Arf6 and Rac1 activities are necessary but not sufficient for ARAP2 to promote the growth of FAs and we speculate that ARAP2 has additional functions that are effector in nature to promote or stabilize FAs.

Indexed as

Signal TransductionADP-Ribosylation Factor 6ADP-Ribosylation FactorsAnimalsCarrier ProteinsCell AdhesionCell LineFocal AdhesionsGene Expression RegulationGlutathione TransferaseGTPase-Activating ProteinsHeLa CellsHumansMicroscopy, ConfocalModels, GeneticMutationADP-Ribosylation Factor 6ADP-Ribosylation FactorsARAP2 protein, humanARF6 protein, humanARFGAP1 protein, humanCarrier ProteinsGlutathione TransferaseGTPase-Activating Proteinsrac1 GTP-Binding ProteinRAC1 protein, humanRNA, Small Interfering

Identifiers

PMID23295182
PMCPMC3581411
OpenAlexW1972422664

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.