Literature DB >> 28377241

Genetic epidemiological study doesn't support GLA IVS4+919G>A variant is a significant mutation in Fabry disease.

Hung-Lun Chiang1, Nana Hsiang-Hua Wang2, I-Wen Song2, Chun-Ping Chang2, Ming-Shien Wen3, Yin-Hsiu Chien4, Wuh-Liang Hwu4, Fuu-Jen Tsai5, Yuan-Tsong Chen6, Jer-Yuarn Wu7.   

Abstract

BACKGROUND: The GLA IVS4+919G>A which is linked to late-onset Fabry disease shows high frequency in Taiwan.
METHODS: To determine whether IVS4+919G>A is a frequent cause of heart disease, we genotyped it in normal controls and other disease cohorts (type 2 diabetes, heart failure, ventricular tachycardia, atrial fibrillation and coronary artery disease). Normal controls and diabetes patients carrying the variant were evaluated for their cardiac condition. Minigene constructs were used to study GLA splicing patterns in different cell lines.
RESULTS: GLA IVS4+919A was found in 4/1634 males (0.245%) and 2/1634 females (0.123%) in normal controls and in 4/2133 males (0.188%) and 7/1816 females (0.385%) in the type 2 diabetes cohort. Of all the 17 IVS4+919A carriers in these two groups, only two males reported heart-related disease (myocardial infarction and hypertensive heart disease). Furthermore, in the heart disease cohort (n=649), only one male carried the variant. Minigene constructs showed that the AGS (stomach) cell line showed a distinct GLA splicing pattern.
CONCLUSION: Most subjects carrying GLA IVS4+919A did not show abnormal cardiac phenotypes. The near-absence of GLA IVS4+919A in heart disease cohort suggested that this variant is not a frequent cause of overt heart diseases in Taiwan and that the genotype-phenotype correlation and natural course of the disease need further investigation. We also showed that the GLA IVS4+919G>A nucleotide change did influence alternative splicing in a tissue-specific manner. SYNOPSIS: The GLA IVS4+919G>A variant is not a frequent cause of overt heart disease in Taiwan.
Copyright © 2017. Published by Elsevier Inc.

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Year:  2017        PMID: 28377241     DOI: 10.1016/j.ymgme.2017.03.005

Source DB:  PubMed          Journal:  Mol Genet Metab        ISSN: 1096-7192            Impact factor:   4.797


  2 in total

1.  Improvement of gastrointestinal symptoms in a significant proportion of male patients with classic Fabry disease treated with agalsidase beta: A Fabry Registry analysis stratified by phenotype.

Authors:  Robert J Hopkin; Ulla Feldt-Rasmussen; Dominique P Germain; Ana Jovanovic; Ana Maria Martins; Kathleen Nicholls; Alberto Ortiz; Juan Politei; Elvira Ponce; Carmen Varas; Frank Weidemann; Meng Yang; William R Wilcox
Journal:  Mol Genet Metab Rep       Date:  2020-10-30

2.  A Novel α-Galactosidase A Splicing Mutation Predisposes to Fabry Disease.

Authors:  Ping Li; Lijuan Zhang; Na Zhao; Qiuhong Xiong; Yong-An Zhou; Changxin Wu; Han Xiao
Journal:  Front Genet       Date:  2019-02-11       Impact factor: 4.599

  2 in total

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