Evidence map›Paper›PMID 18541910›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2008

Bves directly interacts with GEFT, and controls cell shape and movement through regulation of Rac1/Cdc42 activity.

T K Smith, H A Hager, R Francis, D M Kilkenny, C W Lo, D M Bader

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

41 citing papers in PubMed, 62 citations in OpenAlex.

  1. Article
  2. Article
  3. Systemic AAV9.BVES delivery ameliorates muscular dystrophy in a mouse model of LGMDR25.Molecular therapy : the journal of the American Society of Gene Therapy · 2023
    Article
  4. Article
  5. Review
  6. Article
  7. The Role of POPDC Proteins in Cardiac Pacemaking and Conduction.Journal of cardiovascular development and disease · 2021
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. The Functional Polymorphism R129W in theGenetic testing and molecular biomarkers · 2019
    Article
  16. GEFT aberrant expression in soft tissue sarcomas.Translational cancer research · 2019
    Article
  17. Review
  18. Review
  19. Review
  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

6 authors at 3 institutions in 1 country.

T K SmithThe Stahlman Cardiovascular Research Laboratories, Program for Developmental Biology, and Department of Medicine, Vanderbilt University Medical Center, Nashville, TN 37232-6300, USA.
H A Hager
R Francis
D M Kilkenny
C W Lo
D M Bader
Vanderbilt University Medical Center · USNational Heart Lung and Blood Institute · USNational Institutes of Health · US

Funding

Training In Cardiovascular ResearchT32HL007411 · NHLBI · VANDERBILT UNIVERSITY · PI BECKMAN, JOSHUA A · 1985 to 2020
$7.2M
REGULATION OF CARDIAC MYOCYTE DIFFERENTIATIONR01HL037675 · NHLBI · WEILL MEDICAL COLLEGE OF CORNELL UNIV · PI BADER, DAVID M · 1986 to 2017
$4.7M
Bves Function in Cardiac MyogenesisR01HL079050 · NHLBI · VANDERBILT UNIVERSITY · PI BADER, DAVID M · 2006 to 2009
$1.5M
NHLBI NIH HHS HL07411NHLBI NIH HHS HL079050NHLBI NIH HHS HL37675NHLBI NIH HHS HL79050NHLBI NIH HHS R01 HL037675NHLBI NIH HHS R01 HL079050NHLBI NIH HHS T32 HL007411
6 · The paper itself

Abstract

Bves is an integral membrane protein with no determined function and no homology to proteins outside of the Popdc family. It is widely expressed throughout development in myriad organisms. Here, we demonstrate an interaction between Bves and guanine nucleotide exchange factor T (GEFT), a GEF for Rho-family GTPases. This interaction represents the first identification of any protein that has a direct physical interaction with any member of the Popdc family. Bves and GEFT are shown to colocalize in adult skeletal muscle. We also demonstrate that exogenous expression of Bves reduces Rac1 and Cdc42 activity levels while not affecting levels of active RhoA. Consistent with a repression of Rac1 and Cdc42 activity, we show changes in speed of cell locomotion and cell roundness also result from exogenous expression of Bves. Modulation of Rho-family GTPase signaling by Bves would be highly consistent with previously described phenotypes occurring upon disruption of Bves function in a wide variety of model systems. Therefore, we propose Bves as a novel regulator of the Rac1 and Cdc42 signaling cascades.

Indexed as

Cell MovementCell ShapeAnimalscdc42 GTP-Binding ProteinCell Adhesion MoleculesCytoplasmDNA Mutational AnalysisGuanine Nucleotide Exchange FactorsMiceMuscle CellsMuscle ProteinsNeuropeptidesNIH 3T3 CellsProtein Interaction Domains and Motifsrac1 GTP-Binding Proteinrac GTP-Binding ProteinsBves protein, mousecdc42 GTP-Binding ProteinCell Adhesion MoleculesGEFT protein, mouseGuanine Nucleotide Exchange FactorsMuscle ProteinsNeuropeptidesrac1 GTP-Binding ProteinRac1 protein, mouserac GTP-Binding ProteinsRho Guanine Nucleotide Exchange Factors

Identifiers

PMID18541910
PMCPMC2423412
OpenAlexW2007366243

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.