Evidence map›Paper›PMID 21789221›Full record

ArticlePloS one2011

Gene targeting implicates Cdc42 GTPase in GPVI and non-GPVI mediated platelet filopodia formation, secretion and aggregation.

Huzoor Akbar, Xun Shang, Rehana Perveen, Mark Berryman, Kevin Funk, James F Johnson, Narendra N Tandon, Yi Zheng

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

35 citing papers in PubMed, 61 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. The voltage-gated KPlatelets · 2022
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Integrin αBlood · 2017
    Review
  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

8 authors at 3 institutions in 1 country.

Huzoor AkbarDepartment of Biomedical Sciences, College of Osteopathic Medicine, Ohio University, Athens, Ohio, United States of America. akbar@ohio.edu
Xun Shang
Rehana Perveen
Mark Berryman
Kevin Funk
James F Johnson
Narendra N Tandon
Yi Zheng
Ohio University · USUniversity of Cincinnati · USOtsuka (United States) · US

Funding

Rac GTPases as Targets in LymphomagenesisR01CA125658 · NCI · CINCINNATI CHILDRENS HOSP MED CTR · PI ZHENG, YI · 2007 to 2011
$2.1M
Cell Type and Stimulus-Specific Signaling Role of CDC42 in BloodR01HL085362 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI ZHENG, YI · 2006 to 2010
$2.0M
NCI NIH HHS R01 CA125658NCI NIH HHS R01 CA125658 S1NHLBI NIH HHS R01 HL085362
6 · The paper itself

Abstract

backgroundCdc42 and Rac1, members of the Rho family of small GTPases, play critical roles in actin cytoskeleton regulation. We have shown previously that Rac1 is involved in regulation of platelet secretion and aggregation. However, the role of Cdc42 in platelet activation remains controversial. This study was undertaken to better understand the role of Cdc42 in platelet activation. METHODOLOGY/PRINCIPAL

findingsWe utilized the Mx-cre;Cdc42(lox/lox) inducible mice with transient Cdc42 deletion to investigate the involvement of Cdc42 in platelet function. The Cdc42-deficient mice exhibited a significantly reduced platelet count than the matching Cdc42(+/+) mice. Platelets isolated from Cdc42(-/-), as compared to Cdc42(+/+), mice exhibited (a) diminished phosphorylation of PAK1/2, an effector molecule of Cdc42, (b) inhibition of filopodia formation on immobilized CRP or fibrinogen, (c) inhibition of CRP- or thrombin-induced secretion of ATP and release of P-selectin, (d) inhibition of CRP, collagen or thrombin induced platelet aggregation, and (e) minimal phosphorylation of Akt upon stimulation with CRP or thrombin. The bleeding times were significantly prolonged in Cdc42(-/-) mice compared with Cdc42(+/+) mice. CONCLUSION/SIGNIFICANCE: Our data demonstrate that Cdc42 is required for platelet filopodia formation, secretion and aggregation and therefore plays a critical role in platelet mediated hemostasis and thrombosis.

Indexed as

Gene TargetingPlatelet AggregationAnimalsBleeding TimeBlood PlateletsBone MarrowCarrier Proteinscdc42 GTP-Binding ProteinEnzyme ActivationFibrinogenGene DeletionMicep21-Activated KinasesPeptidesPlatelet Membrane GlycoproteinsProto-Oncogene Proteins c-aktCarrier Proteinscdc42 GTP-Binding Proteincollagen-related peptideFibrinogenp21-Activated KinasesPeptidesPlatelet Membrane Glycoproteinsplatelet membrane glycoprotein VIProto-Oncogene Proteins c-aktThrombin

Identifiers

PMID21789221
PMCPMC3138762
OpenAlexW1967409563

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.