Evidence map›Paper›PMID 26483211›Full record

ArticleDevelopment (Cambridge, England)2015

Dach2-Hdac9 signaling regulates reinnervation of muscle endplates.

Peter C D Macpherson, Pershang Farshi, Daniel Goldman

Open access · bronzeAbstract read
In one paragraph

Article in Development (Cambridge, England), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

23 citing papers in PubMed, 36 citations in OpenAlex.

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  16. Long Non-Coding RNANon-coding RNA · 2019
    Article
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  20. Sarcoglycan Alpha Mitigates Neuromuscular Junction Decline in Aged Mice by Stabilizing LRP4.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018
    Article
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

3 authors at 1 institution in 1 country.

Peter C D MacphersonMolecular and Behavioral Neuroscience Institute, Department of Biological Chemistry, University of Michigan, Ann Arbor, MI 48109, USA.
Pershang FarshiMolecular and Behavioral Neuroscience Institute, Department of Biological Chemistry, University of Michigan, Ann Arbor, MI 48109, USA.
Daniel GoldmanMolecular and Behavioral Neuroscience Institute, Department of Biological Chemistry, University of Michigan, Ann Arbor, MI 48109, USA neuroman@umich.edu.
University of Michigan–Ann Arbor · US

Funding

Activity-dependent regulation of neuromuscular junction formationR01NS059848 · NINDS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI GOLDMAN, DANIEL J · 2009 to 2012
$1.3M
NINDS NIH HHS R01 NS059848
6 · The paper itself

Abstract

Muscle denervation resulting from injury, disease or aging results in impaired motor function. Restoring neuromuscular communication requires axonal regrowth and endplate reinnervation. Muscle activity inhibits the reinnervation of denervated muscle. The mechanism by which muscle activity regulates muscle reinnervation is poorly understood. Dach2 and Hdac9 are activity-regulated transcriptional co-repressors that are highly expressed in innervated muscle and suppressed following muscle denervation. Dach2 and Hdac9 control the expression of endplate-associated genes such as those encoding nicotinic acetylcholine receptors (nAChRs). Here we tested the idea that Dach2 and Hdac9 mediate the effects of muscle activity on muscle reinnervation. Dach2 and Hdac9 were found to act in a collaborative fashion to inhibit reinnervation of denervated mouse skeletal muscle and appear to act, at least in part, by inhibiting denervation-dependent induction of Myog and Gdf5 gene expression. Although Dach2 and Hdac9 inhibit Myog and Gdf5 mRNA expression, Myog does not regulate Gdf5 transcription. Thus, Myog and Gdf5 appear to stimulate muscle reinnervation through parallel pathways. These studies suggest that manipulating the Dach2-Hdac9 signaling system, and Gdf5 in particular, might be a good approach for enhancing motor function in instances where neuromuscular communication has been disrupted.

Indexed as

Gene Expression Regulation, DevelopmentalSignal TransductionAnimalsAxonsDNA-Binding ProteinsFemaleGrowth Differentiation Factor 5Histone DeacetylasesMaleMiceMice, KnockoutMicroscopy, FluorescenceMuscle, SkeletalMyogeninNeuronsNuclear ProteinsDach2 protein, mouseDNA-Binding ProteinsGdf5 protein, mouseGrowth Differentiation Factor 5Hdac9 protein, mouseHistone DeacetylasesMyogeninMyog protein, mouseNuclear ProteinsRepressor ProteinsRNA, Small InterferingTranscription FactorsBrachypodiaDach2DenervationGdf5Hdac9Motor nerveMuscleMyogeninNerveNeuromuscular junctionRegeneration

Identifiers

PMID26483211
PMCPMC4712835
OpenAlexW2175816760

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.