The mismatch repair system protects against intergenerational GAA repeat instability in a Friedreich ataxia mouse model.
about
DNA triplet repeat expansion and mismatch repairA MutSβ-Dependent Contribution of MutSα to Repeat Expansions in Fragile X Premutation Mice?Pms2 suppresses large expansions of the (GAA·TTC)n sequence in neuronal tissuesGeneration and characterisation of Friedreich ataxia YG8R mouse fibroblast and neural stem cell modelsDHX9 helicase is involved in preventing genomic instability induced by alternatively structured DNA in human cellsNeurons and cardiomyocytes derived from induced pluripotent stem cells as a model for mitochondrial defects in Friedreich's ataxia.MutLα heterodimers modify the molecular phenotype of Friedreich ataxia.MSH3 polymorphisms and protein levels affect CAG repeat instability in Huntington's disease miceDifferent roles of eukaryotic MutS and MutL complexes in repair of small insertion and deletion loops in yeast.Mismatch repair genes Mlh1 and Mlh3 modify CAG instability in Huntington's disease mice: genome-wide and candidate approachesModifiers of (CAG)(n) instability in Machado-Joseph disease (MJD/SCA3) transmissions: an association study with DNA replication, repair and recombination genes.Repeat instability during DNA repair: Insights from model systemsThe Repeat Expansion Diseases: The dark side of DNA repair.DNA mismatch repair complex MutSβ promotes GAA·TTC repeat expansion in human cellsRole of mismatch repair enzymes in GAA·TTC triplet-repeat expansion in Friedreich ataxia induced pluripotent stem cells.Mutsβ generates both expansions and contractions in a mouse model of the Fragile X-associated disordersMature microsatellites: mechanisms underlying dinucleotide microsatellite mutational biases in human cells.Epigenetics in Friedreich's Ataxia: Challenges and Opportunities for Therapy.Friedreich ataxia: neuropathology revised.Analysis of alternative lengthening of telomere markers in BRCA1 defective cells.The mismatch repair protein MSH2 is rate limiting for repeat expansion in a fragile X premutation mouse model.Expanded complexity of unstable repeat diseases.Gene regulation and epigenetics in Friedreich's ataxia.Animal and cellular models of Friedreich ataxia.The dual nature of mismatch repair as antimutator and mutator: for better or for worse.Replication stalling and DNA microsatellite instability.Close encounters: Moving along bumps, breaks, and bubbles on expanded trinucleotide tracts.Loss of MSH2 and MSH6 due to heterozygous germline defects in MSH3 and MSH6.GAA•TTC repeat expansion in human cells is mediated by mismatch repair complex MutLγ and depends upon the endonuclease domain in MLH3 isoform one.
P2860
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P2860
The mismatch repair system protects against intergenerational GAA repeat instability in a Friedreich ataxia mouse model.
description
2012 nî lūn-bûn
@nan
2012年の論文
@ja
2012年論文
@yue
2012年論文
@zh-hant
2012年論文
@zh-hk
2012年論文
@zh-mo
2012年論文
@zh-tw
2012年论文
@wuu
2012年论文
@zh
2012年论文
@zh-cn
name
The mismatch repair system pro ...... Friedreich ataxia mouse model.
@ast
The mismatch repair system pro ...... Friedreich ataxia mouse model.
@en
type
label
The mismatch repair system pro ...... Friedreich ataxia mouse model.
@ast
The mismatch repair system pro ...... Friedreich ataxia mouse model.
@en
prefLabel
The mismatch repair system pro ...... Friedreich ataxia mouse model.
@ast
The mismatch repair system pro ...... Friedreich ataxia mouse model.
@en
P2093
P2860
P1476
The mismatch repair system pro ...... Friedreich ataxia mouse model.
@en
P2093
Chiranjeevi Sandi
Hein Te Riele
Madhavi Sandi
Mark A Pook
Ricardo Mouro Pinto
Sahar Al-Mahdawi
Vahid Ezzatizadeh
P2860
P304
P356
10.1016/J.NBD.2012.01.002
P577
2012-01-20T00:00:00Z