Excision of the expanded GAA repeats corrects cardiomyopathy phenotypes of iPSC-derived Friedreich's ataxia cardiomyocytes-Reference-Cited by-同舟云学术

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Excision of the expanded GAA repeats corrects cardiomyopathy phenotypes of iPSC-derived Friedreich's ataxia cardiomyocytes

Published:2019-10 Issue: Volume:40 Page:101529
ISSN:1873-5061
Container-title:Stem Cell Research
language:en
Short-container-title:Stem Cell Research

Author:

Li Jixue,Rozwadowska Natalia,Clark Amanda,Fil Daniel,Napierala Jill S.,Napierala Marek

Funder

Muscular Dystrophy Association

National Institutes of Health

National Institute of Neurological Disorders and Stroke

Friedreich's Ataxia Research Alliance

Publisher

Elsevier BV

Subject

Cell Biology,Developmental Biology,General Medicine

Reference56 articles.

1. RNA expression profiling of human iPSC-derived cardiomyocytes in a cardiac hypertrophy model;Aggarwal;PLoS ONE,2014

2. Long noncoding RNAs: cellular address codes in development and disease;Batista;Cell,2013

3. Deep sequencing of mitochondrial genomes reveals increased mutation load in Friedreich's ataxia;Bhalla;Ann. Clin. Transl. Neurol.,2016

4. Frataxin acts as an iron chaperone protein to modulate mitochondrial aconitase activity;Bulteau;Science,2004

5. Friedreich’s ataxia: autosomal recessive disease caused by an intronic GAA triplet repeat expansion;Campuzano;Science,1996

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3. Exploring mitochondrial biomarkers for Friedreich's ataxia: a multifaceted approach;Journal of Neurology;2024-03-23

4. Human frataxin, the Friedreich ataxia deficient protein, interacts with mitochondrial respiratory chain;Cell Death & Disease;2023-12-08

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