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Targeting lipid peroxidation and mitochondrial imbalance in Friedreich's ataxia

Pharmacological research, 2015-09, Vol.99, p.344-350

2015

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Frataxin deficiency leads to defects in expression of antioxidants and Nrf2 expression in dorsal root ganglia of the Friedreich's ataxia YG8R mouse model

Antioxidants & redox signaling, 2013-11, Vol.19 (13), p.1481-1493

2013

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Animal and cellular models of Friedreich ataxia

Journal of neurochemistry, 2013-08, Vol.126 (s1), p.65-79

2013

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The emerging role of 5-hydroxymethylcytosine in neurodegenerative diseases

Frontiers in neuroscience, 2014-12, Vol.8, p.397-397

2014

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Cellular, molecular and functional characterisation of YAC transgenic mouse models of Friedreich ataxia

PloS one, 2014-09, Vol.9 (9), p.e107416-e107416

2014

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Dimethyl fumarate dosing in humans increases frataxin expression: A potential therapy for Friedreich's Ataxia

PloS one, 2019-06, Vol.14 (6), p.e0217776-e0217776

2019

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Generation and characterisation of Friedreich ataxia YG8R mouse fibroblast and neural stem cell models

PloS one, 2014-02, Vol.9 (2), p.e89488

2014

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MutLα heterodimers modify the molecular phenotype of Friedreich ataxia

PloS one, 2014-06, Vol.9 (6), p.e100523

2014

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Novel frataxin isoforms may contribute to the pathological mechanism of Friedreich ataxia

PloS one, 2012-10, Vol.7 (10), p.e47847-e47847

2012

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Friedreich ataxia patient tissues exhibit increased 5-hydroxymethylcytosine modification and decreased CTCF binding at the FXN locus

PloS one, 2013-09, Vol.8 (9), p.e74956-e74956

2013

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Interruptions of the FXN GAA Repeat Tract Delay the Age at Onset of Friedreich’s Ataxia in a Location Dependent Manner

International journal of molecular sciences, 2021-07, Vol.22 (14), p.7507

2021

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Dyclonine rescues frataxin deficiency in animal models and buccal cells of patients with Friedreich's ataxia

Human molecular genetics, 2014-12, Vol.23 (25), p.6848-6862

2014

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A new FRDA mouse model [ Fxn null :YG8s(GAA) > 800] with more than 800 GAA repeats

Frontiers in neuroscience, 2023-01, Vol.17, p.930422-930422

2023

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Pms2 suppresses large expansions of the (GAA·TTC)n sequence in neuronal tissues

PloS one, 2012-10, Vol.7 (10), p.e47085

2012

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Prolonged treatment with pimelic o -aminobenzamide HDAC inhibitors ameliorates the disease phenotype of a Friedreich ataxia mouse model

Neurobiology of disease, 2011-06, Vol.42 (3), p.496-505

2011

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Pharmacological screening using an FXN-EGFP cellular genomic reporter assay for the therapy of Friedreich ataxia

PloS one, 2013-02, Vol.8 (2), p.e55940

2013

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A novel GAA-repeat-expansion-based mouse model of Friedreich's ataxia

Disease models & mechanisms, 2015-03, Vol.8 (3), p.225-235

2015

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Deranged Calcium Signaling and Neurodegeneration in Spinocerebellar Ataxia Type 3

The Journal of neuroscience, 2008-11, Vol.28 (48), p.12713-12724

2008

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Large Interruptions of GAA Repeat Expansion Mutations in Friedreich Ataxia Are Very Rare

Frontiers in cellular neuroscience, 2018-11, Vol.12, p.443-443

2018

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FAST-1 antisense RNA epigenetically alters FXN expression

Scientific reports, 2018-11, Vol.8 (1), p.17217-11, Article 17217

2018

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FXN Promoter Silencing in the Humanized Mouse Model of Friedreich Ataxia

PloS one, 2015-09, Vol.10 (9), p.e0138437-e0138437

2015

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The role of mitochondrial labile iron in Friedreich's ataxia skin fibroblasts sensitivity to ultraviolet A

Metallomics, 2019-03, Vol.11 (3), p.656-665

2019

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DNA methylation in Friedreich ataxia silences expression of frataxin isoform E

Scientific reports, 2022-03, Vol.12 (1), p.5031-14, Article 5031

2022

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GAA repeat expansion mutation mouse models of Friedreich ataxia exhibit oxidative stress leading to progressive neuronal and cardiac pathology

Genomics (San Diego, Calif.), 2006-11, Vol.88 (5), p.580-590

2006

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The mismatch repair system protects against intergenerational GAA repeat instability in a Friedreich ataxia mouse model

Neurobiology of disease, 2012-04, Vol.46 (1), p.165-171

2012

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Targeting lipid peroxidation and mitochondrial imbalance in Friedreich's ataxia

Frataxin deficiency leads to defects in expression of antioxidants and Nrf2 expression in dorsal root ganglia of the Friedreich's ataxia YG8R mouse model

Animal and cellular models of Friedreich ataxia

The emerging role of 5-hydroxymethylcytosine in neurodegenerative diseases

Cellular, molecular and functional characterisation of YAC transgenic mouse models of Friedreich ataxia

Dimethyl fumarate dosing in humans increases frataxin expression: A potential therapy for Friedreich's Ataxia

Generation and characterisation of Friedreich ataxia YG8R mouse fibroblast and neural stem cell models

MutLα heterodimers modify the molecular phenotype of Friedreich ataxia

Novel frataxin isoforms may contribute to the pathological mechanism of Friedreich ataxia

Friedreich ataxia patient tissues exhibit increased 5-hydroxymethylcytosine modification and decreased CTCF binding at the FXN locus

Interruptions of the FXN GAA Repeat Tract Delay the Age at Onset of Friedreich’s Ataxia in a Location Dependent Manner

Dyclonine rescues frataxin deficiency in animal models and buccal cells of patients with Friedreich's ataxia

A new FRDA mouse model [ Fxn null :YG8s(GAA) > 800] with more than 800 GAA repeats

Pms2 suppresses large expansions of the (GAA·TTC)n sequence in neuronal tissues

Prolonged treatment with pimelic o -aminobenzamide HDAC inhibitors ameliorates the disease phenotype of a Friedreich ataxia mouse model

Pharmacological screening using an FXN-EGFP cellular genomic reporter assay for the therapy of Friedreich ataxia

A novel GAA-repeat-expansion-based mouse model of Friedreich's ataxia

Deranged Calcium Signaling and Neurodegeneration in Spinocerebellar Ataxia Type 3

Large Interruptions of GAA Repeat Expansion Mutations in Friedreich Ataxia Are Very Rare

FAST-1 antisense RNA epigenetically alters FXN expression

FXN Promoter Silencing in the Humanized Mouse Model of Friedreich Ataxia

The role of mitochondrial labile iron in Friedreich's ataxia skin fibroblasts sensitivity to ultraviolet A

DNA methylation in Friedreich ataxia silences expression of frataxin isoform E

GAA repeat expansion mutation mouse models of Friedreich ataxia exhibit oxidative stress leading to progressive neuronal and cardiac pathology

The mismatch repair system protects against intergenerational GAA repeat instability in a Friedreich ataxia mouse model

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