Evidence map›Paper›PMID 31394789›Full record

ArticleCells2019

Modulation of Agrin and RhoA Pathways Ameliorates Movement Defects and Synapse Morphology in MYO9A-Depleted Zebrafish.

Emily O'Connor, George Cairns, Sally Spendiff, David Burns, Stefan Hettwer, Armin Mäder, Juliane Müller, Rita Horvath, Clarke Slater, Andreas Roos and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cells, 2019. 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
0.9field-weighted citation impact, top 25% 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
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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

11 authors at 5 institutions in 5 countries.

Emily O'ConnorJohn Walton Muscular Dystrophy Research Centre, MRC Centre for Neuromuscular Diseases, Institute of Genetic Medicine, Newcastle University, Newcastle upon Tyne NE1 3BZ, UK.
George CairnsInterdisciplinary School of Health Sciences, Faculty of Health Sciences, University of Ottawa, Ottawa, ON K1H 8L1, Canada.
Sally SpendiffChildren's Hospital of Eastern Ontario Research Institute, University of Ottawa, Ottawa, ON K1H 8L1, Canada.ORCID 0000-0001-9579-3514
David BurnsInstitute of Cell and Molecular Biosciences, Newcastle University, Newcastle Upon Tyne NE2 4HH, UK.
Stefan HettwerNeurotune AG. Wagistrasse 27a, 8952 Schlieren, Switzerland.
Armin MäderNeurotune AG. Wagistrasse 27a, 8952 Schlieren, Switzerland.
Juliane MüllerDepartment of Clinical Neurosciences, University of Cambridge, Cambridge CB2 0QQ, UK.
Rita HorvathDepartment of Clinical Neurosciences, University of Cambridge, Cambridge CB2 0QQ, UK.
Clarke SlaterInstitute of Neuroscience, Newcastle University, Newcastle Upon Tyne NE2 4HH, UK.
Andreas RoosDepartment of Neuropediatrics, Centre for Neuromuscular Disorders in Children, University Hospital Essen, University of Duisburg-Essen, 45122 Essen, Germany.
Hanns LochmüllerChildren's Hospital of Eastern Ontario Research Institute, University of Ottawa, Ottawa, ON K1H 8L1, Canada. hlochmuller@cheo.on.ca.ORCID 0000-0003-2324-8001
Newcastle University · GBUniversity of Ottawa · CANeurotune (Switzerland) · CHUniversity of Cambridge · GBUniversity of Duisburg-Essen · DE

Funding

CIHR PJT 162265
6 · The paper itself

Abstract

Congenital myasthenic syndromes (CMS) are a group of rare, inherited disorders characterised by impaired function of the neuromuscular junction (NMJ). This is due to defects in one of the many proteins associated with the NMJ. In three patients with CMS, missense mutations in a gene encoding an unconventional myosin protein, MYO9A, were identified as likely causing their disorder. Preliminary studies revealed a potential involvement of the RhoA/ROCK pathway and of a key NMJ protein, agrin, in the pathophysiology of MYO9A-depletion. In this study, a CRISPR/Cas9 approach was used to generate genetic mutants of

Indexed as

Neuromuscular JunctionAnimalsMutation, MissenseMyosinsrho-Associated KinasesZebrafishMyosinsrho-Associated KinasesfasudilMyo9aaMyo9abmyosin IXaneuromuscular junctionNT1654unconventional myosin

Identifiers

PMID31394789
PMCPMC6721702
OpenAlexW2965838536

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.