Evidence map›Paper›PMID 37231228›Full record

ArticleNeurogenetics2023

COLQ-related congenital myasthenic syndrome: An integrative view.

Tina Eshaghian, Bahareh Rabbani, Reza Shervin Badv, Sahar Mikaeeli, Behdad Gharib, Stanley Iyadurai, Nejat Mahdieh

Abstract read
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In one paragraph

Article in Neurogenetics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
1.4field-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

2 citing papers in PubMed, 7 citations in OpenAlex.

  1. Enhanced multistress tolerance ofMicrobiology spectrum · 2025
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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

7 authors at 4 institutions in 2 countries.

Tina Eshaghian *Growth and Development Research, Tehran University of Medical Sciences, Tehran, Iran.
Bahareh Rabbani *Growth and Development Research, Tehran University of Medical Sciences, Tehran, Iran.
Reza Shervin BadvGrowth and Development Research, Tehran University of Medical Sciences, Tehran, Iran.
Sahar MikaeeliGrowth and Development Research, Tehran University of Medical Sciences, Tehran, Iran.
Behdad GharibChildren's Hospital Center, Pediatric Center of Excellence, Tehran University of Medical Center, Tehran, Iran.
Stanley IyaduraiJohns Hopkins All Children's Hospital, Division of Neurology, 601 5th Street S, St. Petersburg, FL, 33701, USA.
Nejat MahdiehGrowth and Development Research, Tehran University of Medical Sciences, Tehran, Iran. nmahdieh@yahoo.com.ORCID http://orcid.org/0000-0002-8614-1538
Tehran University of Medical Sciences · IRUniversity of Tehran · IRIran University of Medical Sciences · IRJohns Hopkins University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Congenital myasthenic syndromes are inherited disorders caused by mutation in components of the neuromuscular junction and manifest early in life. Mutations in COLQ gene result in congenital myasthenic syndrome. Here, we present the analysis of data from 209 patients from 195 unrelated families highlighting genotype-phenotype correlation. In addition, we describe a COLQ homozygous variant a new patient and discuss it utilizing the Phyre2 and I-TASSER programs. Clinical, molecular genetics, imaging (MRI), and electrodiagnostic (EEG, EMG/NCS) evaluations were performed. Our data showed 89 pathogenic/likely pathogenic variants including 35 missenses, 21 indels, 14 nonsense, 14 splicing, and 5 large deletions variants. Eight common variants were responsible for 48.46% of those. Weakness in proximal muscles, hypotonia, and generalized weakness were detected in all individuals tested. Apart from the weakness, extensive clinical heterogeneity was noted among patients with COLQ-related patients based on their genotypes-those with variants affecting the splice site exhibited more severe clinical features while those with missense variants displayed milder phenotypes, suggesting the role of differential splice variants in multiple functions within the muscle. Analyses and descriptions of these COLQ variants may be helpful in clinical trial readiness and potential development of novel therapies in the setting of established structure-function relationships.

Indexed as

Myasthenic Syndromes, CongenitalAcetylcholinesteraseCollagenGenotypeHumansMuscle ProteinsMutationMutation, MissensePhenotypeAcetylcholinesteraseCollagenCOLQ protein, humanMuscle ProteinsCMSCOLQcongenital myasthenic syndromesIn silico analysisIranian populationTina Eshaghian and Bahareh Rabbani are first authors and contributed equally to this work.

Identifiers

PMID37231228
OpenAlexW4378194045

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.