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Patterns of CAG repeat instability in the central nervous system and periphery in Huntington’s disease and in spinocerebellar ataxia type 1

Human molecular genetics, 2020-08, Vol.29 (15), p.2551-2567

2020

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Somatic CAG expansion in Huntington's disease is dependent on the MLH3 endonuclease domain, which can be excluded via splice redirection

Nucleic acids research, 2021-04, Vol.49 (7), p.3907

2021

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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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Histone deacetylase knockouts modify transcription, CAG instability and nuclear pathology in Huntington disease mice

eLife, 2020-09, Vol.9

2020

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Promotion of somatic CAG repeat expansion by Fan1 knock-out in Huntington’s disease knock-in mice is blocked by Mlh1 knock-out

Human molecular genetics, 2020-11, Vol.29 (18), p.3044-3053

2020

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Mismatch repair genes Mlh1 and Mlh3 modify CAG instability in Huntington's disease mice: genome-wide and candidate approaches

PLoS genetics, 2013-10, Vol.9 (10), p.e1003930

2013

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The Friedreich ataxia GAA repeat expansion mutation induces comparable epigenetic changes in human and transgenic mouse brain and heart tissues

Human molecular genetics, 2008-03, Vol.17 (5), p.735-746

2008

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Splice modulators target PMS1 to reduce somatic expansion of the Huntington's disease-associated CAG repeat

Nature communications, 2024-04, Vol.15 (1), p.3182-3182, Article 3182

2024

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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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Quantification of age-dependent somatic CAG repeat instability in Hdh CAG knock-in mice reveals different expansion dynamics in striatum and liver

PloS one, 2011-08, Vol.6 (8), p.e23647-e23647

2011

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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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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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Age-Dependent Increase in Tau Phosphorylation at Serine 396 in Huntington's Disease Prefrontal Cortex

Journal of Huntington's disease, 2023-01, Vol.12 (3), p.267

2023

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GAA repeat instability in Friedreich ataxia YAC transgenic mice

Genomics (San Diego, Calif.), 2004-08, Vol.84 (2), p.301-310

2004

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Assessing average somatic CAG repeat instability at the protein level

Scientific reports, 2019-12, Vol.9 (1), p.19152-14, Article 19152

2019

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Genetic Risk Underlying Psychiatric and Cognitive Symptoms in Huntington’s Disease

Biological psychiatry (1969), 2020-05, Vol.87 (9), p.857-865

2020

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Genetic Contributors to Intergenerational CAG Repeat Instability in Huntington's Disease Knock-In Mice

Genetics (Austin), 2017-02, Vol.205 (2), p.503-516

2017

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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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Pms2 Suppresses Large Expansions of the .sub.n Sequence in Neuronal Tissues

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

2012

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Pms2 Suppresses Large Expansions of the

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

2012

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Mismatch Repair Genes Mlh1 and Mlh3 Modify CAG Instability in Huntington's Disease Mice: Genome-Wide and Candidate Approaches: e1003930

PLoS genetics, 2013-10, Vol.9 (10)

2013

Volltextzugriff (PDF)

Friedreich Ataxia Patient Tissues Exhibit Increased 5-Hydroxymethylcytosine Modification and Decreased CTCF Binding at the FXN Locus: e74956

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

2013

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Therapeutic testing and epigenetic characterization of friedreich ataxia

Mouro Pinto, Ricardo

2009

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Patterns of CAG repeat instability in the central nervous system and periphery in Huntington’s disease and in spinocerebellar ataxia type 1

Somatic CAG expansion in Huntington's disease is dependent on the MLH3 endonuclease domain, which can be excluded via splice redirection

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

Histone deacetylase knockouts modify transcription, CAG instability and nuclear pathology in Huntington disease mice

Identification of Genetic Factors that Modify Clinical Onset of Huntington’s Disease

Promotion of somatic CAG repeat expansion by Fan1 knock-out in Huntington’s disease knock-in mice is blocked by Mlh1 knock-out

Mismatch repair genes Mlh1 and Mlh3 modify CAG instability in Huntington's disease mice: genome-wide and candidate approaches

The Friedreich ataxia GAA repeat expansion mutation induces comparable epigenetic changes in human and transgenic mouse brain and heart tissues

Splice modulators target PMS1 to reduce somatic expansion of the Huntington's disease-associated CAG repeat

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

Quantification of age-dependent somatic CAG repeat instability in Hdh CAG knock-in mice reveals different expansion dynamics in striatum and liver

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

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

Age-Dependent Increase in Tau Phosphorylation at Serine 396 in Huntington's Disease Prefrontal Cortex

GAA repeat instability in Friedreich ataxia YAC transgenic mice

CAG Repeat Not Polyglutamine Length Determines Timing of Huntington’s Disease Onset

Assessing average somatic CAG repeat instability at the protein level

Genetic Risk Underlying Psychiatric and Cognitive Symptoms in Huntington’s Disease

Genetic Contributors to Intergenerational CAG Repeat Instability in Huntington's Disease Knock-In Mice

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

Pms2 Suppresses Large Expansions of the .sub.n Sequence in Neuronal Tissues

Pms2 Suppresses Large Expansions of the

Mismatch Repair Genes Mlh1 and Mlh3 Modify CAG Instability in Huntington's Disease Mice: Genome-Wide and Candidate Approaches: e1003930

Friedreich Ataxia Patient Tissues Exhibit Increased 5-Hydroxymethylcytosine Modification and Decreased CTCF Binding at the FXN Locus: e74956

Therapeutic testing and epigenetic characterization of friedreich ataxia

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