c.376A>G, (p.S126G) Alpha Galactosidase A Mutation Induces ER Stress, Unfolded Protein Response and Reduced Enzyme Transport to Lysosome: Possible  Relevance in the Pathogenesis of Late Onset Forms of Fabry Disease-Reference-Cited by-同舟云学术

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c.376A>G, (p.S126G) Alpha Galactosidase A Mutation Induces ER Stress, Unfolded Protein Response and Reduced Enzyme Transport to Lysosome: Possible  Relevance in the Pathogenesis of Late Onset Forms of Fabry Disease

Published:2023 Issue: Volume: Page:
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Author:

Riillo Concetta,Bonapace Giuseppe,Moricca Maria Teresa,Sestito Simona,Salatino Alessandro,Concolino Daniela

Publisher

Elsevier BV

Reference35 articles.

1. The pathophysiology of Fabry disease;S Olivera-Gonzalez;Rev Clin Esp (Barc),2018

2. The molecular defect leading to Fabry disease: structure of human alpha-galactosidase;S C Garman;J Mol Biol,2004

3. Clinical and diagnostic aspects of Fabry disease management: a narrative review with a particular focus on Brazilian experts' perspectives;R Giugliani;Journal of Inborn Errors of Metabolism and Screening,2022

4. Clinical Characteristics, Renal Involvement, and Therapeutic Options of Pediatric Patients With Fabry Disease;C Muntean;Front Pediatr,2022

5. The heart in Anderson-Fabry disease;S Sestito;Journal of biological regulators and homeostatic agents,2020

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