Exenatide induces frataxin expression and improves mitochondrial function in Friedreich ataxia-Reference-Cited by-同舟云学术

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Exenatide induces frataxin expression and improves mitochondrial function in Friedreich ataxia

Published:2020-01-30 Issue:2 Volume:5 Page:
ISSN:2379-3708
Container-title:JCI Insight
language:en
Short-container-title:

Author:

Igoillo-Esteve Mariana,Oliveira Ana F.,Cosentino Cristina,Fantuzzi Federica,Demarez Céline,Toivonen Sanna,Hu Amélie,Chintawar Satyan,Lopes Miguel^ORCID,Pachera Nathalie,Cai Ying,Abdulkarim Baroj^ORCID,Rai Myriam,Marselli Lorella^ORCID,Marchetti Piero,Tariq Mohammad,Jonas Jean-Christophe^ORCID,Boscolo Marina,Pandolfo Massimo^ORCID,Eizirik Décio L.,Cnop Miriam^ORCID

Funder

Fonds Erasme

Friedreich Ataxia Research Alliance

European Union’s Horizon 2020 research and innovation programme

Brussels Region Innoviris

Fonds National de la Recherche Scientifique

Publisher

American Society for Clinical Investigation

Subject

General Medicine

Link

https://insight.jci.org/articles/view/134221/files/pdf

Reference80 articles.

1. Friedreich's Ataxia: Autosomal Recessive Disease Caused by an Intronic GAA Triplet Repeat Expansion

2. DNA triplet repeats mediate heterochromatin-protein-1-sensitive variegated gene silencing

3. Expanded GAA repeats impair FXN gene expression and reposition the FXN locus to the nuclear lamina in single cells

4. Histone deacetylase inhibitors reverse gene silencing in Friedreich's ataxia

5. The Friedreich ataxia GAA repeat expansion mutation induces comparable epigenetic changes in human and transgenic mouse brain and heart tissues;Al-Mahdawi;Hum Mol Genet,2008

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