Triplet repeat mutation length gains correlate with cell-type specific vulnerability in Huntington disease brain. - Wikidata - awgldk - TriplyDB

Triplet repeat mutation length gains correlate with cell-type specific vulnerability in Huntington disease brain.

Triplet repeat mutation length gains correlate with cell-type specific vulnerability in Huntington disease brain.

http://www.wikidata.org/entity/Q33281163

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Continuous and periodic expansion of CAG repeats in Huntington's disease R6/1 mice Pms2 suppresses large expansions of the (GAA·TTC)n sequence in neuronal tissues GFP-based fluorescence assay for CAG repeat instability in cultured human cells Unusual structures are present in DNA fragments containing super-long Huntingtin CAG repeats Isolated short CTG/CAG DNA slip-outs are repaired efficiently by hMutSbeta, but clustered slip-outs are poorly repaired.Stoichiometry of base excision repair proteins correlates with increased somatic CAG instability in striatum over cerebellum in Huntington's disease transgenic mice DNA instability in replicating Huntington's disease lymphoblasts A novel approach to investigate tissue-specific trinucleotide repeat instability.Intergenerational and striatal CAG repeat instability in Huntington's disease knock-in mice involve different DNA repair genes The pathogenic exon 1 HTT protein is produced by incomplete splicing in Huntington's disease patients Striatal Vulnerability in Huntington's Disease: Neuroprotection Versus Neurotoxicity.Topoisomerase 1 and single-strand break repair modulate transcription-induced CAG repeat contraction in human cells.A selective inhibitor of histone deacetylase 3 prevents cognitive deficits and suppresses striatal CAG repeat expansions in Huntington's disease mice Differential vulnerability of neurons in Huntington's disease: the role of cell type-specific features.Quantification of age-dependent somatic CAG repeat instability in Hdh CAG knock-in mice reveals different expansion dynamics in striatum and liver Xpa deficiency reduces CAG trinucleotide repeat instability in neuronal tissues in a mouse model of SCA1.Histone deacetylase complexes promote trinucleotide repeat expansions Msh2 acts in medium-spiny striatal neurons as an enhancer of CAG instability and mutant huntingtin phenotypes in Huntington's disease knock-in mice Bidirectional transcription stimulates expansion and contraction of expanded (CTG)*(CAG) repeats.Transcription elongation and tissue-specific somatic CAG instability.Role of transcript and interplay between transcription and replication in triplet-repeat instability in mammalian cells.Huntington's disease mouse models online: high-resolution MRI images with stereotaxic templates for computational neuroanatomy MSH3 polymorphisms and protein levels affect CAG repeat instability in Huntington's disease mice Mismatch repair genes Mlh1 and Mlh3 modify CAG instability in Huntington's disease mice: genome-wide and candidate approaches Mechanisms of trinucleotide repeat instability during human development Stabilization of expanded (CTG)•(CAG) repeats by antisense oligonucleotides.CAG repeat lengths > or =335 attenuate the phenotype in the R6/2 Huntington's disease transgenic mouse.The Repeat Expansion Diseases: The dark side of DNA repair.Searching for non-B DNA-forming motifs using nBMST (non-B DNA motif search tool)The nucleotide sequence, DNA damage location, and protein stoichiometry influence the base excision repair outcome at CAG/CTG repeats Effects of Anthocyanins on CAG Repeat Instability and Behaviour in Huntington's Disease R6/1 Mice.Evolving Notch polyQ tracts reveal possible solenoid interference elements DNA instability in postmitotic neurons.Neil1 is a genetic modifier of somatic and germline CAG trinucleotide repeat instability in R6/1 mice.Problems and solutions for the analysis of somatic CAG repeat expansion and their relationship to Huntington's disease toxicity.Full-length human mutant huntingtin with a stable polyglutamine repeat can elicit progressive and selective neuropathogenesis in BACHD mice.E. coli mismatch repair acts downstream of replication fork stalling to stabilize the expanded (GAA.TTC)(n) sequence.Somatic expansion of the Huntington's disease CAG repeat in the brain is associated with an earlier age of disease onset.Hyperactivity and cortical disinhibition in mice with restricted expression of mutant huntingtin to parvalbumin-positive cells.A brief history of triplet repeat diseases.

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P2860

Triplet repeat mutation length gains correlate with cell-type specific vulnerability in Huntington disease brain.

http://www.wikidata.org/entity/Q33281163

description

2007 nî lūn-bûn

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2007 թուականի Ապրիլին հրատարակուած գիտական յօդուած

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2007 թվականի ապրիլին հրատարակված գիտական հոդված

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2007年の論文

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Triplet repeat mutation length ...... y in Huntington disease brain.

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Triplet repeat mutation length ...... y in Huntington disease brain.

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Triplet repeat mutation length ...... y in Huntington disease brain.

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Triplet repeat mutation length ...... y in Huntington disease brain.

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Triplet repeat mutation length ...... y in Huntington disease brain.

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Triplet repeat mutation length ...... y in Huntington disease brain.

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Triplet repeat mutation length ...... y in Huntington disease brain.

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Triplet repeat mutation length ...... y in Huntington disease brain.

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Triplet repeat mutation length ...... y in Huntington disease brain.

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Human Molecular Genetics

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Christine Keller-McGandy

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Jean Paul Vonsattel

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Louis Dubeau

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Nancy S Wexler

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Nicola J Veitch

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Norman Arnheim

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Peggy F Shelbourne

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Song-Ro Yoon

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US-Venezuela Collaborative Research Group

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1133-1142

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10.1093/HMG/DDM054

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10

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16

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17409200

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Huntington disease