Evidence map›Paper›PMID 33199701›Full record

ArticleNature communications2020

Vav2 catalysis-dependent pathways contribute to skeletal muscle growth and metabolic homeostasis.

Sonia Rodríguez-Fdez, L Francisco Lorenzo-Martín, Isabel Fernández-Pisonero, Begoña Porteiro, Christelle Veyrat-Durebex, Daniel Beiroa, Omar Al-Massadi, Antonio Abad, Carlos Diéguez, Roberto Coppari and 2 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2020. 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
1.6field-weighted citation impact, top 16% 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, 36 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. The Rho guanine dissociation inhibitor α inhibits skeletal muscle Rac1 activity and insulin action.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Review
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

12 authors at 3 institutions in 2 countries.

Sonia Rodríguez-FdezCentro de Investigaación del Cáncer, CSIC-University of Salamanca, 37007, Salamanca, Spain.ORCID 0000-0001-5369-2969
L Francisco Lorenzo-MartínCentro de Investigaación del Cáncer, CSIC-University of Salamanca, 37007, Salamanca, Spain.ORCID 0000-0003-4717-9338
Isabel Fernández-PisoneroCentro de Investigaación del Cáncer, CSIC-University of Salamanca, 37007, Salamanca, Spain.ORCID 0000-0002-5130-2143
Begoña PorteiroDepartamento de Fisioloxía, University of Santiago de Compostela, 15782, Santiago de Compostela, Spain.
Christelle Veyrat-DurebexDepartment of Cell Physiology and Metabolism, Faculty of Medicine, University of Geneva, 1211, Geneva, Switzerland.
Daniel BeiroaDepartamento de Fisioloxía, University of Santiago de Compostela, 15782, Santiago de Compostela, Spain.
Omar Al-MassadiDepartamento de Fisioloxía, University of Santiago de Compostela, 15782, Santiago de Compostela, Spain.
Antonio AbadCentro de Investigaación del Cáncer, CSIC-University of Salamanca, 37007, Salamanca, Spain.
Carlos DiéguezDepartamento de Fisioloxía, University of Santiago de Compostela, 15782, Santiago de Compostela, Spain.
Roberto CoppariDepartment of Cell Physiology and Metabolism, Faculty of Medicine, University of Geneva, 1211, Geneva, Switzerland.
Rubén NogueirasDepartamento de Fisioloxía, University of Santiago de Compostela, 15782, Santiago de Compostela, Spain.ORCID 0000-0002-9976-9930
Xosé R BusteloCentro de Investigaación del Cáncer, CSIC-University of Salamanca, 37007, Salamanca, Spain. xbustelo@usal.es.ORCID 0000-0001-9398-6072
Universidad de Salamanca · ESUniversidade de Santiago de Compostela · ESUniversity of Geneva · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Skeletal muscle promotes metabolic balance by regulating glucose uptake and the stimulation of multiple interorgan crosstalk. We show here that the catalytic activity of Vav2, a Rho GTPase activator, modulates the signaling output of the IGF1- and insulin-stimulated phosphatidylinositol 3-kinase pathway in that tissue. Consistent with this, mice bearing a Vav2 protein with decreased catalytic activity exhibit reduced muscle mass, lack of proper insulin responsiveness and, at much later times, a metabolic syndrome-like condition. Conversely, mice expressing a catalytically hyperactive Vav2 develop muscle hypertrophy and increased insulin responsiveness. Of note, while hypoactive Vav2 predisposes to, hyperactive Vav2 protects against high fat diet-induced metabolic imbalance. These data unveil a regulatory layer affecting the signaling output of insulin family factors in muscle.

Indexed as

BiocatalysisHomeostasisMetabolismSignal TransductionAdipocytes, WhiteAdipose Tissue, BrownAnimalsBody CompositionBody WeightCell LineCell SizeGenotypeGlucoseInsulinInsulin-Like Growth Factor IMice, Inbred C57BLGlucoseInsulinInsulin-Like Growth Factor IPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-vavrac1 GTP-Binding ProteinVav2 protein, mouse

Identifiers

PMID33199701
PMCPMC7669868
OpenAlexW3103131650

What Socratic 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 Socratic graph.