Evidence map›Paper›PMID 30995108›Full record

ArticleAmerican journal of physiology. Cell physiology2019

Differential YAP nuclear signaling in healthy and dystrophic skeletal muscle.

Shama R Iyer, Sameer B Shah, Christopher W Ward, Joseph P Stains, Espen E Spangenburg, Eric S Folker, Richard M Lovering

Open access · bronzeAbstract read
In one paragraph

Article in American journal of physiology. Cell physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.8field-weighted citation impact, top 17% 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

19 citing papers in PubMed, 26 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Skeletal Muscle-SpecificInternational journal of molecular sciences · 2023
    Article
  5. Article
  6. Review
  7. Article
  8. Dystrophin missense mutations alter focal adhesion tension and mechanotransduction.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  9. Review
  10. The Neuromuscular Junction: Roles in Aging and Neuromuscular Disease.International journal of molecular sciences · 2021
    Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Molecular Mechanisms of Skeletal Muscle Hypertrophy.Journal of neuromuscular diseases · 2021
    Review
  16. Review
  17. Review
  18. Article
  19. Integrin signaling: linking mechanical stimulation to skeletal muscle hypertrophy.American journal of physiology. Cell physiology · 2019
    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

7 authors at 4 institutions in 1 country.

Shama R IyerDepartment of Orthopaedics, University of Maryland School of Medicine , Baltimore, Maryland.
Sameer B ShahDepartment of Orthopaedic Surgery, University of California San Diego , La Jolla, California.
Christopher W WardDepartment of Orthopaedics, University of Maryland School of Medicine , Baltimore, Maryland.
Joseph P StainsDepartment of Orthopaedics, University of Maryland School of Medicine , Baltimore, Maryland.
Espen E SpangenburgDepartment of Physiology, East Carolina Diabetes and Obesity Institute, East Carolina University , Greenville, North Carolina.
Eric S FolkerDepartment of Biology, Boston College , Chestnut Hill, Massachusetts.
Richard M LoveringDepartment of Orthopaedics, University of Maryland School of Medicine , Baltimore, Maryland.ORCID 0000-0002-9899-5071
University of Maryland, Baltimore · USBoston College · USEast Carolina University · USUniversity of California San Diego · US

Funding

Interdisciplinary Training Program Muscle BiologyT32AR007592 · NIAMS · UNIVERSITY OF MARYLAND BALTIMORE · PI Aikaterini Kontrogianni-Konstantopoulos · 1996 to 2026
$11.7M
Mechanisms of Force Loss in Injured and Dystrophic Skeletal MuscleR01AR059179 · NIAMS · UNIVERSITY OF MARYLAND BALTIMORE · PI LOVERING, RICHARD M · 2010 to 2014
$1.4M
Targeting of cells to musculoskeletal injury via superparamagenetic nanoparticlesR21AR067872 · NIAMS · UNIVERSITY OF MARYLAND BALTIMORE · PI LOVERING, RICHARD M · 2016 to 2017
$373k
NIAMS NIH HHS R01 AR059179NIAMS NIH HHS R21 AR067872NIAMS NIH HHS T32 AR007592
6 · The paper itself

Abstract

Mechanical forces regulate muscle development, hypertrophy, and homeostasis. Force-transmitting structures allow mechanotransduction at the sarcolemma, cytoskeleton, and nuclear envelope. There is growing evidence that Yes-associated protein (YAP) serves as a nuclear relay of mechanical signals and can induce a range of downstream signaling cascades. Dystrophin is a sarcolemma-associated protein, and its absence underlies the pathology in Duchenne muscular dystrophy. We tested the hypothesis that the absence of dystrophin in muscle would result in reduced YAP signaling in response to loading. Following in vivo contractile loading in muscles of healthy (wild-type; WT) mice and mice lacking dystrophin (

Indexed as

Mechanotransduction, CellularMuscle ContractionActive Transport, Cell NucleusAdaptor Proteins, Signal TransducingAnimalsCell Cycle ProteinsDisease Models, AnimalDystrophinMice, Inbred mdxMuscle, SkeletalMuscular Dystrophy, AnimalPhosphorylationYAP-Signaling ProteinsAdaptor Proteins, Signal Transducingapo-dystrophin 1Cell Cycle ProteinsDystrophinYap1 protein, mouseYAP-Signaling Proteinsdystrophymechanotransductionskeletal muscle

Identifiers

PMID30995108
PMCPMC6689751
OpenAlexW2937860081

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.