Cockayne syndrome B protein antagonizes OGG1 in modulating CAG repeat length in vivo.
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Suppression of Somatic Expansion Delays the Onset of Pathophysiology in a Mouse Model of Huntington’s DiseaseThe chicken or the egg: mitochondrial dysfunction as a cause or consequence of toxicity in Huntington's diseaseGFP-based fluorescence assay for CAG repeat instability in cultured human cellsGender and cell-type-specific effects of the transcription-coupled repair protein, ERCC6/CSB, on repeat expansion in a mouse model of the fragile X-related disordersTopoisomerase 1 and single-strand break repair modulate transcription-induced CAG repeat contraction in human cells.Xpa deficiency reduces CAG trinucleotide repeat instability in neuronal tissues in a mouse model of SCA1.Cockayne syndrome protein A is a transcription factor of RNA polymerase I and stimulates ribosomal biogenesis and growthNucleotide excision repair, mismatch repair, and R-loops modulate convergent transcription-induced cell death and repeat instabilityMSH3 polymorphisms and protein levels affect CAG repeat instability in Huntington's disease miceDNA polymerase β deficiency leads to neurodegeneration and exacerbates Alzheimer disease phenotypes.Modifiers of (CAG)(n) instability in Machado-Joseph disease (MJD/SCA3) transmissions: an association study with DNA replication, repair and recombination genes.The transcription-coupled repair protein ERCC6/CSB also protects against repeat expansion in a mouse model of the fragile X premutation.Repeat instability during DNA repair: Insights from model systemsThe Repeat Expansion Diseases: The dark side of DNA repair.Chromatin changes in the development and pathology of the Fragile X-associated disorders and Friedreich ataxia.Trinucleotide repeat deletion via a unique hairpin bypass by DNA polymerase β and alternate flap cleavage by flap endonuclease 1.Neil1 is a genetic modifier of somatic and germline CAG trinucleotide repeat instability in R6/1 mice.Bidirectional transcription of trinucleotide repeats: roles for excision repair.Crosstalk between MSH2-MSH3 and polβ promotes trinucleotide repeat expansion during base excision repair.Abnormal base excision repair at trinucleotide repeats associated with diseases: a tissue-selective mechanism.Nuclear and mitochondrial DNA repair in selected eukaryotic aging model systems.The yin and yang of repair mechanisms in DNA structure-induced genetic instability.Impact of alternative DNA structures on DNA damage, DNA repair, and genetic instabilityClose encounters: Moving along bumps, breaks, and bubbles on expanded trinucleotide tracts.Age-related length variability of polymorphic CAG repeats.The central role of DNA damage and repair in CAG repeat diseases.The Chromatin Remodeler Isw1 Prevents CAG Repeat Expansions During Transcription in Saccharomyces cerevisiae.
P2860
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P2860
Cockayne syndrome B protein antagonizes OGG1 in modulating CAG repeat length in vivo.
description
2011 nî lūn-bûn
@nan
2011 թուականի Մայիսին հրատարակուած գիտական յօդուած
@hyw
2011 թվականի մայիսին հրատարակված գիտական հոդված
@hy
2011年の論文
@ja
2011年論文
@yue
2011年論文
@zh-hant
2011年論文
@zh-hk
2011年論文
@zh-mo
2011年論文
@zh-tw
2011年论文
@wuu
name
Cockayne syndrome B protein antagonizes OGG1 in modulating CAG repeat length in vivo.
@ast
Cockayne syndrome B protein antagonizes OGG1 in modulating CAG repeat length in vivo.
@en
type
label
Cockayne syndrome B protein antagonizes OGG1 in modulating CAG repeat length in vivo.
@ast
Cockayne syndrome B protein antagonizes OGG1 in modulating CAG repeat length in vivo.
@en
prefLabel
Cockayne syndrome B protein antagonizes OGG1 in modulating CAG repeat length in vivo.
@ast
Cockayne syndrome B protein antagonizes OGG1 in modulating CAG repeat length in vivo.
@en
P2093
P2860
P356
P1433
P1476
Cockayne syndrome B protein antagonizes OGG1 in modulating CAG repeat length in vivo.
@en
P2093
Cynthia T McMurray
Irina V Kovtun
Kurt O Johnson
P2860
P304
P356
10.18632/AGING.100324
P577
2011-05-01T00:00:00Z