OGG1 initiates age-dependent CAG trinucleotide expansion in somatic cells - Wikidata - awgldk - TriplyDB

OGG1 initiates age-dependent CAG trinucleotide expansion in somatic cells

OGG1 initiates age-dependent CAG trinucleotide expansion in somatic cells

http://www.wikidata.org/entity/Q37189455

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The excitatory neurotransmitter glutamate stimulates DNA repair to increase neuronal resiliency Fragile X syndrome: the FMR1 CGG repeat distribution among world populations CAG expansion in the Huntington disease gene is associated with a specific and targetable predisposing haplogroup Epigenetic principles and mechanisms underlying nervous system functions in health and disease Tumor-specific microsatellite instability: do distinct mechanisms underlie the MSI-L and EMAST phenotypes?DNA triplet repeat expansion and mismatch repair PGC-1α, mitochondrial dysfunction, and Huntington's disease Repeat-mediated genetic and epigenetic changes at the FMR1 locus in the Fragile X-related disorders Genetics and neuropathology of Huntington's disease Suppression of Somatic Expansion Delays the Onset of Pathophysiology in a Mouse Model of Huntington’s Disease Continuous and periodic expansion of CAG repeats in Huntington's disease R6/1 mice Postreplicative mismatch repair.The 26S proteasome drives trinucleotide repeat expansions Rapid unwinding of triplet repeat hairpins by Srs2 helicase of Saccharomyces cerevisiae Expansion, mosaicism and interruption: mechanisms of the CAG repeat mutation in spinocerebellar ataxia type 1 The chicken or the egg: mitochondrial dysfunction as a cause or consequence of toxicity in Huntington's disease Ups and Downs: Mechanisms of Repeat Instability in the Fragile X-Related Disorders APE1 incision activity at abasic sites in tandem repeat sequences Base excision repair Role of oxidative DNA damage in mitochondrial dysfunction and Huntington's disease pathogenesis A role for oxidized DNA precursors in Huntington's disease-like striatal neurodegeneration Instability of CTG repeats is governed by the position of a DNA base lesion through base excision repair GFP-based fluorescence assay for CAG repeat instability in cultured human cells MutSβ promotes trinucleotide repeat expansion by recruiting DNA polymerase β to nascent (CAG)n or (CTG)n hairpins for error-prone DNA synthesis Identification of hepta-histidine as a candidate drug for Huntington's disease by in silico-in vitro- in vivo-integrated screens of chemical libraries Isolated short CTG/CAG DNA slip-outs are repaired efficiently by hMutSbeta, but clustered slip-outs are poorly repaired.Systems biology analysis of Drosophila in vivo screen data elucidates core networks for DNA damage repair in SCA1.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 Diverse effects of individual mismatch repair components on transcription-induced CAG repeat instability in human cells.Progressive GAA.TTC repeat expansion in human cell lines.A novel approach to investigate tissue-specific trinucleotide repeat instability.Base excision repair of tandem modifications in a methylated CpG dinucleotide.Double-strand break repair pathways protect against CAG/CTG repeat expansions, contractions and repeat-mediated chromosomal fragility in Saccharomyces cerevisiae Convergent transcription through a long CAG tract destabilizes repeats and induces apoptosis HMGB1: roles in base excision repair and related function.Modulation of trinucleotide repeat instability by DNA polymerase β polymorphic variant R137Q.Mechanistic studies of hairpin to duplex conversion for trinucleotide repeat sequences.Mutant huntingtin impairs Ku70-mediated DNA repair.Interrogating the "unsequenceable" genomic trinucleotide repeat disorders by long-read sequencing

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OGG1 initiates age-dependent CAG trinucleotide expansion in somatic cells

http://www.wikidata.org/entity/Q37189455

description

article científic

@ca

article scientifique

@fr

articolo scientifico

@it

artigo científico

@pt

bilimsel makale

@tr

scientific article published on 22 April 2007

@en

vedecký článok

@sk

vetenskaplig artikel

@sv

videnskabelig artikel

@da

vědecký článek

@cs

name

OGG1 initiates age-dependent CAG trinucleotide expansion in somatic cells

@en

OGG1 initiates age-dependent CAG trinucleotide expansion in somatic cells.

@nl

type

label

OGG1 initiates age-dependent CAG trinucleotide expansion in somatic cells

@en

OGG1 initiates age-dependent CAG trinucleotide expansion in somatic cells.

@nl

prefLabel

OGG1 initiates age-dependent CAG trinucleotide expansion in somatic cells

@en

OGG1 initiates age-dependent CAG trinucleotide expansion in somatic cells.

@nl

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OGG1 initiates age-dependent CAG trinucleotide expansion in somatic cells

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Cynthia T McMurray

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Irina V Kovtun

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

Samuel H Wilson

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

Yuan Liu

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

P2860

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Identification and characterization of a human DNA glycosylase for repair of modified bases in oxidatively damaged DNA

Accumulation of premutagenic DNA lesions in mice defective in removal of oxidative base damage

Cloning and expression in Escherichia coli of the OGG1 gene of Saccharomyces cerevisiae, which codes for a DNA glycosylase that excises 7,8-dihydro-8-oxoguanine and 2,6-diamino-4-hydroxy-5-N-methylformamidopyrimidine

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Contribution of DNA sequence and CAG size to mutation frequencies of intermediate alleles for Huntington disease: evidence from single sperm analyses

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

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447-452

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scholarly article

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10.1038/NATURE05778

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7143

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Magnar Bjørås

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2007-04-22T00:00:00Z

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6379045

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1035707745

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17450122

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2681094

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