Evidence map›Paper›PMID 25605336›Full record

ArticleMolecular and cellular biology2015

Muscle-derived extracellular signal-regulated kinases 1 and 2 are required for the maintenance of adult myofibers and their neuromuscular junctions.

Bonnie Seaberg, Gabrielle Henslee, Shuo Wang, Ximena Paez-Colasante, Gary E Landreth, Mendell Rimer

Open access · bronzeAbstract read
In one paragraph

Article in Molecular and cellular biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

24 citing papers in PubMed, 29 citations in OpenAlex.

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  19. Sarcopenia: Aging-Related Loss of Muscle Mass and Function.Physiological reviews · 2019 · on this map
    Review
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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.

Bonnie SeabergDepartment of Neuroscience and Experimental Therapeutics, College of Medicine, Texas A&M University Health Science Center, Bryan, Texas, USA.
Gabrielle HensleeDepartment of Neuroscience and Experimental Therapeutics, College of Medicine, Texas A&M University Health Science Center, Bryan, Texas, USA.
Shuo WangDepartment of Neuroscience and Experimental Therapeutics, College of Medicine, Texas A&M University Health Science Center, Bryan, Texas, USA.
Ximena Paez-ColasanteDepartment of Neuroscience and Experimental Therapeutics, College of Medicine, Texas A&M University Health Science Center, Bryan, Texas, USA Texas A&M University Institute for Neuroscience, College Station, Texas, USA.
Gary E LandrethDepartment of Neurosciences, Case Western Reserve University School of Medicine, Cleveland, Ohio, USA.
Mendell RimerDepartment of Neuroscience and Experimental Therapeutics, College of Medicine, Texas A&M University Health Science Center, Bryan, Texas, USA Texas A&M University Institute for Neuroscience, College Station, Texas, USA mjrimer@medicine.tamhsc.edu.
Texas A&M Health Science Center · USTexas A&M University · USUniversity School · US

Funding

Role of ERK1/2 in Neuromuscular Synapses and Myofiber Development in vivoR21NS077177 · NINDS · TEXAS A&M UNIVERSITY HEALTH SCIENCE CTR · PI RIMER, MENDELL · 2012 to 2013
$387k
NINDS NIH HHS NS077177NINDS NIH HHS R21 NS077177
6 · The paper itself

Abstract

The Ras-extracellular signal-regulated kinase 1 and 2 (ERK1/2) pathway appears to be important for the development, maintenance, aging, and pathology of mammalian skeletal muscle. Yet no gene targeting of Erk1/2 in muscle fibers in vivo has been reported to date. We combined a germ line Erk1 mutation with Cre-loxP Erk2 inactivation in skeletal muscle to produce, for the first time, mice lacking ERK1/2 selectively in skeletal myofibers. Animals lacking muscle ERK1/2 displayed stunted postnatal growth, muscle weakness, and a shorter life span. Their muscles examined in this study, sternomastoid and tibialis anterior, displayed fragmented neuromuscular synapses and a mixture of modest fiber atrophy and loss but failed to show major changes in fiber type composition or absence of cell surface dystrophin. Whereas the lack of only ERK1 had no effects on the phenotypes studied, the lack of myofiber ERK2 explained synaptic fragmentation in the sternomastoid but not the tibialis anterior and a decrease in the expression of the acetylcholine receptor (AChR) epsilon subunit gene mRNA in both muscles. A reduction in AChR protein was documented in line with the above mRNA results. Evidence of partial denervation was found in the sternomastoid but not the tibialis anterior. Thus, myofiber ERK1/2 are differentially required for the maintenance of myofibers and neuromuscular synapses in adult mice.

Indexed as

AnimalsFemaleGene DeletionMaleMiceMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Muscle Fibers, SkeletalMuscle, SkeletalNeuromuscular JunctionReceptors, CholinergicMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Receptors, Cholinergic

Identifiers

PMID25605336
PMCPMC4355524
OpenAlexW2049064322

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.