Evidence map›Paper›PMID 27566547›Full record

ArticleThe Journal of biological chemistry2016

Skeletal Muscle-specific G Protein-coupled Receptor Kinase 2 Ablation Alters Isolated Skeletal Muscle Mechanics and Enhances Clenbuterol-stimulated Hypertrophy.

Benjamin P Woodall, Meryl C Woodall, Timothy S Luongo, Laurel A Grisanti, Douglas G Tilley, John W Elrod, Walter J Koch

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.6field-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

5 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Role of G protein-coupled receptor kinases (GRKs) in βPharmacology research & perspectives · 2024
    Article
  3. Review
  4. Review
  5. Molecular Mechanisms of Skeletal Muscle Hypertrophy.Journal of neuromuscular diseases · 2021
    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 1 institution in 1 country.

Benjamin P WoodallFrom the Center for Translational Medicine, Lewis Katz School of Medicine, Temple University, Philadelphia, Pennsylvania 19140-4106.
Meryl C WoodallFrom the Center for Translational Medicine, Lewis Katz School of Medicine, Temple University, Philadelphia, Pennsylvania 19140-4106.
Timothy S LuongoFrom the Center for Translational Medicine, Lewis Katz School of Medicine, Temple University, Philadelphia, Pennsylvania 19140-4106.
Laurel A GrisantiFrom the Center for Translational Medicine, Lewis Katz School of Medicine, Temple University, Philadelphia, Pennsylvania 19140-4106.
Douglas G TilleyFrom the Center for Translational Medicine, Lewis Katz School of Medicine, Temple University, Philadelphia, Pennsylvania 19140-4106.
John W ElrodFrom the Center for Translational Medicine, Lewis Katz School of Medicine, Temple University, Philadelphia, Pennsylvania 19140-4106.
Walter J KochFrom the Center for Translational Medicine, Lewis Katz School of Medicine, Temple University, Philadelphia, Pennsylvania 19140-4106 walter.koch@temple.edu.
Temple University · US

Funding

Training and education CoreU54AR052646 · NIAMS · UNIVERSITY OF PENNSYLVANIA · PI MCNALLY, ELIZABETH M, SWEENEY, H LEE · 2005 to 2020
$24.1M
Targeted Cancer Therapeutics and Heart Failure: Mechanisms and Post-injury RepairP01HL091799 · NHLBI · THOMAS JEFFERSON UNIVERSITY · PI KOCH, WALTER J. · 2008 to 2018
$23.1M
Project 3 Dysregulation of metabolic communication of oligodendrocytes and neurons by cocaine and TatP01DA037830 · NIDA · TEMPLE UNIV OF THE COMMONWEALTH · PI KHALILI, KAMEL · 2015 to 2019
$7.4M
Targeting GRK2 (BARK1) in Heart FailureR37HL061690 · NHLBI · THOMAS JEFFERSON UNIVERSITY · PI KOCH, WALTER J. · 2009 to 2018
$3.9M
Mechanisms of mitochondrial calcium exchange in heart failureR01HL123966 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI ELROD, JOHN WILLIAM · 2014 to 2018
$2.3M
NHLBI NIH HHS P01 HL091799NIAMS NIH HHS U54 AR052646
6 · The paper itself

Abstract

GRK2, a G protein-coupled receptor kinase, plays a critical role in cardiac physiology. Adrenergic receptors are the primary target for GRK2 activity in the heart; phosphorylation by GRK2 leads to desensitization of these receptors. As such, levels of GRK2 activity in the heart directly correlate with cardiac contractile function. Furthermore, increased expression of GRK2 after cardiac insult exacerbates injury and speeds progression to heart failure. Despite the importance of this kinase in both the physiology and pathophysiology of the heart, relatively little is known about the role of GRK2 in skeletal muscle function and disease. In this study we generated a novel skeletal muscle-specific GRK2 knock-out (KO) mouse (MLC-Cre:GRK2

Indexed as

AnimalsClenbuterolG-Protein-Coupled Receptor Kinase 2HypertrophyMiceMice, KnockoutMuscle ContractionMuscle, SkeletalMuscular DiseasesProto-Oncogene Proteins c-aktReceptors, Adrenergic, beta-2Signal TransductionClenbuterolG-Protein-Coupled Receptor Kinase 2GRK2 protein, mouseProto-Oncogene Proteins c-aktReceptors, Adrenergic, beta-2adrenergic receptorAkt PKBG protein-coupled receptor (GPCR)mousemuscle hypertrophymuscle physiology

Identifiers

PMID27566547
PMCPMC5063976
OpenAlexW2517078262

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.