DNA instability in postmitotic neurons. - Wikidata - wikimedia - TriplyDB

DNA instability in postmitotic neurons.

DNA instability in postmitotic neurons.

http://www.wikidata.org/entity/Q36491349

about

PCNA function in the activation and strand direction of MutLα endonuclease in mismatch repair RAN translation and frameshifting as translational challenges at simple repeats of human neurodegenerative disorders Iron dysregulation in Huntington's disease DNA triplet repeat expansion and mismatch repair Continuous and periodic expansion of CAG repeats in Huntington's disease R6/1 mice Ups and Downs: Mechanisms of Repeat Instability in the Fragile X-Related Disorders Unusual structures are present in DNA fragments containing super-long Huntingtin CAG repeats Trinucleotide repeats: a structural perspective Stoichiometry of base excision repair proteins correlates with increased somatic CAG instability in striatum over cerebellum in Huntington's disease transgenic mice CTCF cis-regulates trinucleotide repeat instability in an epigenetic manner: a novel basis for mutational hot spot determination.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 Proteolysis of mutant huntingtin produces an exon 1 fragment that accumulates as an aggregated protein in neuronal nuclei in Huntington disease.A selective inhibitor of histone deacetylase 3 prevents cognitive deficits and suppresses striatal CAG repeat expansions in Huntington's disease mice Quantification of age-dependent somatic CAG repeat instability in Hdh CAG knock-in mice reveals different expansion dynamics in striatum and liver Instability of the octarepeat region of the human prion protein gene.RNA-protein interactions in unstable microsatellite diseases.Msh2 acts in medium-spiny striatal neurons as an enhancer of CAG instability and mutant huntingtin phenotypes in Huntington's disease knock-in mice Cell lineage analysis in human brain using endogenous retroelements.Mismatch repair genes Mlh1 and Mlh3 modify CAG instability in Huntington's disease mice: genome-wide and candidate approaches Microsatellite repeat instability and neurological disease.Mechanisms of trinucleotide repeat instability during human development The transcription-coupled repair protein ERCC6/CSB also protects against repeat expansion in a mouse model of the fragile X premutation.Making (anti-) sense out of huntingtin levels in Huntington disease.Repeat instability during DNA repair: Insights from model systems Large expansion of CTG•CAG repeats is exacerbated by MutSβ in human cells.Instability of (CTG)n•(CAG)n trinucleotide repeats and DNA synthesis The Repeat Expansion Diseases: The dark side of DNA repair.DNA mismatch repair complex MutSβ promotes GAA·TTC repeat expansion in human cells MutSβ and histone deacetylase complexes promote expansions of trinucleotide repeats in human cells.CGG-repeat length and neuropathological and molecular correlates in a mouse model for fragile X-associated tremor/ataxia syndrome.DNA repair pathways underlie a common genetic mechanism modulating onset in polyglutamine diseases Extrahelical (CAG)/(CTG) triplet repeat elements support proliferating cell nuclear antigen loading and MutLα endonuclease activation Inhibition of DNA synthesis facilitates expansion of low-complexity repeats: is strand slippage stimulated by transient local depletion of specific dNTPs?Somatic expansion of the Huntington's disease CAG repeat in the brain is associated with an earlier age of disease onset.Coordination between polymerase beta and FEN1 can modulate CAG repeat expansion.Abnormal base excision repair at trinucleotide repeats associated with diseases: a tissue-selective mechanism.Expression levels of DNA replication and repair genes predict regional somatic repeat instability in the brain but are not altered by polyglutamine disease protein expression or age.

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P2860

DNA instability in postmitotic neurons.

http://www.wikidata.org/entity/Q36491349

description

2008 nî lūn-bûn

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2008年の論文

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2008年学术文章

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2008年学术文章

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2008年学术文章

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2008年学术文章

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2008年学术文章

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2008年學術文章

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2008年學術文章

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2008年學術文章

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name

DNA instability in postmitotic neurons.

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DNA instability in postmitotic neurons.

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DNA instability in postmitotic neurons.

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DNA instability in postmitotic neurons.

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DNA instability in postmitotic neurons.

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DNA instability in postmitotic neurons.

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Proceedings of the National Academy of Sciences of the United States of America

P1476

DNA instability in postmitotic neurons.

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P2093

Ben Woodman

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Hilary Moffitt

http://www.w3.org/2001/XMLSchema#string

Kirupa Sathasivam

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Peter J Detloff

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Richard L M Faull

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Roman Gonitel

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P2860

The origin of mutants

Msh2 deficiency prevents in vivo somatic instability of the CAG repeat in Huntington disease transgenic mice

Neurological abnormalities in a knock-in mouse model of Huntington's disease

Reversal of neuropathology and motor dysfunction in a conditional model of Huntington's disease

Dramatic mutation instability in HD mouse striatum: does polyglutamine load contribute to cell-specific vulnerability in Huntington's disease?

Molecular origins of rapid and continuous morphological evolution

Mammalian neural stem cells

Exon 1 of the HD gene with an expanded CAG repeat is sufficient to cause a progressive neurological phenotype in transgenic mice

The threshold for polyglutamine-expansion protein aggregation and cellular toxicity is dynamic and influenced by aging in Caenorhabditis elegans

Single cell analysis of CAG repeat in brains of dentatorubral-pallidoluysian atrophy (DRPLA).

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5551950

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18299573

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2265187

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