Evidence map›Paper›PMID 23606743›Full record

ArticleJournal of cell science2013

Regulation of IRS1/Akt insulin signaling by microRNA-128a during myogenesis.

Norio Motohashi, Matthew S Alexander, Yuko Shimizu-Motohashi, Jennifer A Myers, Genri Kawahara, Louis M Kunkel

Abstract read
In one paragraph

Article in Journal of cell science, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed, 2 pooled it
5.5field-weighted citation impact, top 3% 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

69 citing papers in PubMed, 2 syntheses or guidelines pooled it, 136 citations in OpenAlex.

  1. Pooled it
  2. Four pleiotropic loci associated with fat mass and lean mass.International journal of obesity (2005) · 2020
    Pooled it
  3. Trial
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  8. Advances in the Regulation of Lipid Metabolism by Non-Coding RNAs.Animals : an open access journal from MDPI · 2025
    Review
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9 more citing papers are in PubMed but not listed here.

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 2 institutions in 1 country.

Norio MotohashiProgram in Genomics, Department of Pediatrics, Boston Children's Hospital, Boston, MA 02115, USA.
Matthew S Alexander
Yuko Shimizu-Motohashi
Jennifer A Myers
Genri Kawahara
Louis M Kunkel
Boston Children's Hospital · USHarvard University · US

Funding

SYNAPTIC MECHANISMS IN HIPPOCAMPAL EPILEPTOGENESISP30HD018655 · NICHD · CHILDREN'S HOSPITAL BOSTON · PI POMEROY, SCOTT LOREN · 1985 to 2015
$26.2M
Progenitor Cells inHuman Skeletal MuscleP50NS040828 · NINDS · BOSTON CHILDREN'S HOSPITAL · PI KOHANE, ISAAC S. · 2008 to 2011
$5.9M
NICHD NIH HHS 2P30HD018655-26NICHD NIH HHS P30 HD018655NICHD NIH HHS P30-HD18655NINDS NIH HHS 5P50NS040828NINDS NIH HHS P50 NS040828
6 · The paper itself

Abstract

Skeletal muscle possesses a strong ability to regenerate following injury, a fact that has been largely attributed to satellite cells. Satellite cells are skeletal muscle stem cells located beneath the basal lamina of the myofiber, and are the principal cellular source of growth and regeneration in skeletal muscle. MicroRNAs (miRNAs) play key roles in modulating several cellular processes by targeting multiple mRNAs that comprise a single or multiple signaling pathway. Several miRNAs have been shown to regulate satellite cell activity, such as miRNA-489, which functions to maintain satellite cells in a quiescent state. Although muscle-specific miRNAs have been identified, many of the molecular mechanisms that regulate myogenesis that are regulated by miRNAs still remain unknown. In this study, we have shown that miR-128a is highly expressed in brain and skeletal muscle, and increases during myoblast differentiation. MiR-128a was found to regulate the target genes involved in insulin signaling, which include Insr (insulin receptor), Irs1 (insulin receptor substrate 1) and Pik3r1 (phosphatidylinositol 3-kinases regulatory 1) at both the mRNA and protein level. Overexpression of miR-128a in myoblasts inhibited cell proliferation by targeting IRS1. By contrast, inhibition of miR-128a induced myotube maturation and myofiber hypertrophy in vitro and in vivo. Moreover, our results demonstrate that miR-128a expression levels are negatively controlled by tumor necrosis factor α (TNF-α). TNF-α promoted myoblast proliferation and myotube hypertrophy by facilitating IRS1/Akt signaling via a direct decrease of miR-128a expression in both myoblasts and myotubes. In summary, we demonstrate that miR-128a regulates myoblast proliferation and myotube hypertrophy, and provides a novel mechanism through which IRS1-dependent insulin signaling is regulated in skeletal muscle.

Indexed as

AnimalsBrainCell DifferentiationCell Growth ProcessesCells, CulturedFemaleHypertrophyInsulinInsulin Receptor Substrate ProteinsMiceMicroRNAsMuscle DevelopmentMuscle Fibers, SkeletalMuscle, SkeletalMyoblastsPhosphatidylinositol 3-KinasesInsulinInsulin Receptor Substrate ProteinsIrs1 protein, mouseMicroRNAsMirn128 microRNA, mousePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReceptor, InsulinTumor Necrosis Factor-alphaCell proliferationInsulin signallingmicroRNAMuscle satellite cellMuscular dystrophy

Identifiers

PMID23606743
PMCPMC3687700
OpenAlexW1976971215

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.