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HA novel approach to investigate tissue-specific trinucleotide repeat instability.
- Published in:
- BMC Systems Biology, 2010, v. 4, p. 29, doi. 10.1186/1752-0509-4-29
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- Article
Histone deacetylase knockouts modify transcription, CAG instability and nuclear pathology in Huntington disease mice.
- Published in:
- eLife, 2020, p. 1, doi. 10.7554/eLife.55911
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- Article
Histone deacetylase knockouts modify transcription, CAG instability and nuclear pathology in Huntington disease mice.
- Published in:
- eLife, 2020, p. 1
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- Article
Large-scale phenome analysis defines a behavioral signature for Huntington's disease genotype in mice.
- Published in:
- Nature Biotechnology, 2016, v. 34, n. 8, p. 838, doi. 10.1038/nbt.3587
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- Article
Population-specific genetic modification of Huntington's disease in Venezuela.
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- PLoS Genetics, 2018, v. 14, n. 5, p. 1, doi. 10.1371/journal.pgen.1007274
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- Article
Corrigendum: Motivational, proteostatic and transcriptional deficits precede synapse loss, gliosis and neurodegeneration in the B6.Htt<sup>Q111/+</sup> model of Huntington's disease.
- Published in:
- Scientific Reports, 2017, p. 44960, doi. 10.1038/srep44960
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- Article
Motivational, proteostatic and transcriptional deficits precede synapse loss, gliosis and neurodegeneration in the B6.Htt<sup>Q111/+</sup> model of Huntington's disease.
- Published in:
- Scientific Reports, 2017, p. 41570, doi. 10.1038/srep41570
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- Article
Splice modulators target PMS1 to reduce somatic expansion of the Huntington's disease-associated CAG repeat.
- Published in:
- Nature Communications, 2024, v. 15, n. 1, p. 1, doi. 10.1038/s41467-024-47485-0
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- Article
HD CAGnome: A Search Tool for Huntingtin CAG Repeat Length-Correlated Genes.
- Published in:
- PLoS ONE, 2014, v. 9, n. 4, p. 1, doi. 10.1371/journal.pone.0095556
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- Article
Msh2Acts in Medium-Spiny Striatal Neurons as an Enhancer of CAG Instability and Mutant Huntingtin Phenotypes in Huntington's Disease Knock-In Mice.
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- PLoS ONE, 2012, v. 7, n. 9, p. 1, doi. 10.1371/journal.pone.0044273
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- Article
Quantification of Age-Dependent Somatic CAG Repeat Instability in Hdh CAG Knock-In Mice Reveals Different Expansion Dynamics in Striatum and Liver.
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- PLoS ONE, 2011, v. 6, n. 8, p. 1, doi. 10.1371/journal.pone.0023647
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- Article
Base editing strategies to convert CAG to CAA diminish the disease-causing mutation in Huntington’s disease.
- Published in:
- eLife, 2024, p. 1, doi. 10.7554/eLife.89782
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- Publication type:
- Article
Assessing average somatic CAG repeat instability at the protein level.
- Published in:
- Scientific Reports, 2019, v. 9, n. 1, p. 1, doi. 10.1038/s41598-019-55202-x
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- Article
Transcriptional regulatory networks underlying gene expression changes in Huntington's disease.
- Published in:
- Molecular Systems Biology, 2018, v. 14, n. 3, p. 1, doi. 10.15252/msb.20167435
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- Article
CAG repeat expansion in the Huntington's disease gene shapes linear and circular RNAs biogenesis.
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- PLoS Genetics, 2023, v. 19, n. 10, p. 1, doi. 10.1371/journal.pgen.1010988
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- Article
Modification of Huntington's disease by short tandem repeats.
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- Brain Communications, 2024, v. 6, n. 2, p. 1, doi. 10.1093/braincomms/fcae016
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- Article
Promotion of somatic CAG repeat expansion by Fan1 knock-out in Huntington's disease knock-in mice is blocked by Mlh1 knock-out.
- Published in:
- Human Molecular Genetics, 2020, v. 29, n. 18, p. 3044, doi. 10.1093/hmg/ddaa196
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- Article
A modifier of Huntington's disease onset at the MLH1 locus.
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- Human Molecular Genetics, 2017, v. 26, n. 19, p. 3859, doi. 10.1093/hmg/ddx286
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- Article
Dominant effects of the Huntington's disease HTT CAG repeat length are captured in gene-expression data sets by a continuous analysis mathematical modeling strategy.
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- Human Molecular Genetics, 2013, v. 22, n. 16, p. 3227, doi. 10.1093/hmg/ddt176
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- Article
Differential effects of the Huntington's disease CAG mutation in striatum and cerebellum are quantitative not qualitative.
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- Human Molecular Genetics, 2011, v. 20, n. 21, p. 4258, doi. 10.1093/hmg/ddr355
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- Article
Genetic Contributors to Intergenerational CAG Repeat Instability in Huntington's Disease Knock-In Mice.
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- Genetics, 2017, v. 205, n. 2, p. 503, doi. 10.1534/genetics.116.195578
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- Article
Somatic CAG expansion in Huntington's disease is dependent on the MLH3 endonuclease domain, which can be excluded via splice redirection.
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- Nucleic Acids Research, 2021, v. 49, n. 7, p. 3907, doi. 10.1093/nar/gkab152
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- Article
Mismatch Repair Genes <i>Mlh1</i> and <i>Mlh3</i> Modify CAG Instability in Huntington's Disease Mice: Genome-Wide and Candidate Approaches.
- Published in:
- PLoS Genetics, 2013, v. 9, n. 10, p. 1, doi. 10.1371/journal.pgen.1003930
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- Article
Stoichiometry of Base Excision Repair Proteins Correlates with Increased Somatic CAG Instability in Striatum over Cerebellum in Huntington's Disease Transgenic Mice.
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- PLoS Genetics, 2009, v. 5, n. 12, p. 1, doi. 10.1371/journal.pgen.1000749
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- Article
Huntingtin facilitates polycomb repressive complex 2.
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- Human Molecular Genetics, 2010, v. 19, n. 4, p. 573, doi. 10.1093/hmg/ddp524
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- Article
Somatic expansion of the Huntington's disease CAG repeat in the brain is associated with an earlier age of disease onset.
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- Human Molecular Genetics, 2009, v. 18, n. 16, p. 3039, doi. 10.1093/hmg/ddp242
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- Article
Genetic background modifies nuclear mutant huntingtin accumulation and HD CAG repeat instability in Huntington's disease knock-in mice.
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- Human Molecular Genetics, 2006, v. 15, n. 12, p. 2015, doi. 10.1093/hmg/ddl125
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- Article
Specific progressive cAMP reduction implicates energy deficit in presymptomatic Huntington's disease knock-in mice.
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- Human Molecular Genetics, 2003, v. 12, n. 5, p. 497, doi. 10.1093/hmg/ddg046
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- Article
Mismatch repair gene Msh2 modifies the timing of early disease in HdhQ111 striatum.
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- Human Molecular Genetics, 2003, v. 12, n. 3, p. 273, doi. 10.1093/hmg/ddg056
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- Article
Identification of a presymptomatic molecular phenotype in Hdh CAG knock-in mice.
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- Human Molecular Genetics, 2002, v. 11, n. 19, p. 2233, doi. 10.1093/hmg/11.19.2233
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- Article
Early phenotypes that presage late-onset neurodegenerative disease allow testing of modifiers in Hdh CAG knock-in mice.
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- Human Molecular Genetics, 2002, v. 11, n. 6, p. 633, doi. 10.1093/hmg/11.6.633
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- Article
The HD mutation causes progressivelethal neurological disease in mice expressing reduced levels ofhuntingtin.
- Published in:
- Human Molecular Genetics, 2001, v. 10, n. 22, p. 2515, doi. 10.1093/hmg/10.22.2515
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- Article
Long glutamine tracts cause nuclear localization of a novel form of huntingtin in medium spiny striatal neurons in Hdh [sup Q92] and Hdh [sup Q111] knock-in mice.
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- Human Molecular Genetics, 2000, v. 9, n. 4, p. 503, doi. 10.1093/hmg/9.4.503
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- Article
Length-dependent gametic CAG repeat instability in the Huntington's disease knock-in mouse.
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- Human Molecular Genetics, 1999, v. 8, n. 1, p. 115, doi. 10.1093/hmg/8.1.115
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- Article