Evidence map›Paper›PMID 32504392›Full record

ArticleMetabolic brain disease2020

GAA gene mutation detection following clinical evaluation and enzyme activity analysis in Azeri Turkish patients with Pompe disease.

Jalal Gharesouran, Abbas Jalaiei, Aida Hosseinzadeh, Soudeh Ghafouri-Fard, Zeinab Mokhtari, Kazem Ghahremanzadeh, Narges Rezazadeh, Shadi Shiva, Shahram Sadeghvand, Mohammad Taheri and 1 more

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In one paragraph

Article in Metabolic brain disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.2field-weighted citation impact, top 45% 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

3 citing papers in PubMed, 3 citations in OpenAlex.

  1. Article
  2. Pompe disease in China: clinical and molecular characteristics.Frontiers in cardiovascular medicine · 2023
    Article
  3. 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

11 authors at 3 institutions in 1 country.

Jalal GharesouranMolecular Genetics Division, GMG center, Tabriz, Iran.
Abbas JalaieiDepartment of Medical Genetics, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran.
Aida HosseinzadehMolecular Genetics Division, GMG center, Tabriz, Iran.
Soudeh Ghafouri-FardDepartment of Medical Genetics, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Zeinab MokhtariAlzahra Hospital, Tabriz University of Medical Sciences, Tabriz, Iran.
Kazem GhahremanzadehChildren Hospital, Tabriz University of Medical Sciences, Tabriz, Iran.
Narges RezazadehDepartment of Animal Biology, Faculty of Natural Sciences, University of Tabriz, Tabriz, Iran.
Shadi ShivaPediatric Health Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Shahram SadeghvandPediatric Health Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Mohammad TaheriUrogenital Stem Cell Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Mohammad_823@yahoo.com.ORCID http://orcid.org/0000-0001-8381-0591
Maryam RezazadehDivision of Medical Genetics, Tabriz Children's Hospital, Tabriz University of Medical Sciences, Tabriz, Iran. Rezazadehm@tbzmed.ac.ir.
Tabriz University of Medical Sciences · IRShahid Beheshti University of Medical Sciences · IRUniversity of Tabriz · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pompe disease (PD) is a rare autosomal recessive multi-systemic lysosomal storage disorder, caused by mutations in the acid alpha-glucosidase (GAA) gene located on 17q25.2-q25.3. It is one of about 50 rare genetic diseases categorized as lysosomal storage disorders. This disease is characterized by a range of different symptoms related to acid alpha-glucosidase deficiency. Mutation recognition in the GAA gene can be very significant for purposes such as therapeutic interference, early diagnosis and genotype-phenotype relationship. In the current study, peripheral blood samples were gathered from patients with PD and healthy members of three families. Enzymatic activity of GAA was checked. Then, mutation detection was performed by polymerase chain reaction followed by direct sequencing of all exons in samples with decreased enzyme activity. The identified mutations were investigated using bioinformatics tools to predict possible effects on the protein product and also to compare the mutated sequence with near species. Three novel mutations (c.1966-1968delGAG, c.2011-2012delAT and c.1475-1481dupACCCCAC) were identified in the GAA gene. Assessment of the effects of these mutations on protein structure and function showed the possibility of harmful effects and their significant alterations in the protein structure. The three novel GAA gene mutations detected in this study expand the information about the molecular genetics of PD and can be used to helpdiagnosis and genetic counseling of affected families.

Indexed as

MutationAdolescentalpha-GlucosidasesChildChild, PreschoolDNA Mutational AnalysisFemaleGenetic Predisposition to DiseaseGlycogenGlycogen Storage Disease Type IIHumansInfantMaleTurkeyalpha-GlucosidasesGlycogenGAA geneNovel mutationPompe disease

Identifiers

PMID32504392
OpenAlexW3033274272

What OpenQuestion holds

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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.