Frataxin-deficient neurons and mice models of Friedreich ataxia are improved by TAT-MTScs-FXN treatment
Author:
Affiliation:
1. Departament de Ciències Mèdiques Bàsiques; IRBLleida; Universitat de Lleida; Lleida Spain
2. BioBlast-Pharma Ltd.; TelAviv Israel
3. The Jackson Laboratory; Bar Harbor Maine USA
Funder
Ministerio de Economía y Competitividad
Federación Española de Enfermedades Raras
Publisher
Wiley
Subject
Cell Biology,Molecular Medicine
Link
http://onlinelibrary.wiley.com/wol1/doi/10.1111/jcmm.13365/fullpdf
Reference48 articles.
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2. Friedreich's ataxia: pathology, pathogenesis, and molecular genetics;Koeppen;J Neurol Sci,2011
3. Friedreich's ataxia: autosomal recessive disease caused by an intronic GAA triplet repeat expansion;Campuzano;Science,1996
4. Frataxin is reduced in Friedreich ataxia patients and is associated with mitochondrial membranes;Campuzano;Hum Mol Genet,1997
5. Friedreich's ataxia protein: phylogenetic evidence for mitochondrial dysfunction;Gibson;Trends Neurosci,1996
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