Cloned human FMR1 trinucleotide repeats exhibit a length- and orientation-dependent instability suggestive of in vivo lagging strand secondary structure.
about
Fragile X (CGG)n repeats induce a transcriptional repression in cis upon a linked promoter: evidence for a chromatin mediated effectDNA triplet repeat expansion and mismatch repairDNA Replication Dynamics of the GGGGCC Repeat of the C9orf72 Gene.Exploring possible DNA structures in real-time polymerase kinetics using Pacific Biosciences sequencer dataMethylation mosaicism of 5'-(CGG)(n)-3' repeats in fragile X, premutation and normal individuals.Stability of the human fragile X (CGG)(n) triplet repeat array in Saccharomyces cerevisiae deficient in aspects of DNA metabolism.Potassium bromate, a potent DNA oxidizing agent, exacerbates germline repeat expansion in a fragile X premutation mouse modelCis-elements governing trinucleotide repeat instability in Saccharomyces cerevisiae.Double-strand breaks in the myotonic dystrophy type 1 and the fragile X syndrome triplet repeat sequences induce different types of mutations in DNA flanking sequences in Escherichia coli.Hijacking of the mismatch repair system to cause CAG expansion and cell death in neurodegenerative disease.An origin of DNA replication in the promoter region of the human fragile X mental retardation (FMR1) geneDeficiency of RecA-dependent RecFOR and RecBCD pathways causes increased instability of the (GAA*TTC)n sequence when GAA is the lagging strand template.Repair of DNA double-strand breaks within the (GAA*TTC)n sequence results in frequent deletion of the triplet-repeat sequenceATR protects the genome against CGG.CCG-repeat expansion in Fragile X premutation mice.Features of trinucleotide repeat instability in vivo.Epigenetics, autism spectrum, and neurodevelopmental disorders.Mutation spectra in fragile X syndrome induced by deletions of CGG*CCG repeats.Translation of the FMR1 mRNA is not influenced by AGG interruptionsTranscription influences the types of deletion and expansion products in an orientation-dependent manner from GAC*GTC repeatsCpG methylation modifies the genetic stability of cloned repeat sequences.Replication-mediated instability of the GAA triplet repeat mutation in Friedreich ataxia.Role of replication and CpG methylation in fragile X syndrome CGG deletions in primate cells.Analysis of human flap endonuclease 1 mutants reveals a mechanism to prevent triplet repeat expansion.Of Men and Mice: Modeling the Fragile X Syndrome.
P2860
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P2860
Cloned human FMR1 trinucleotide repeats exhibit a length- and orientation-dependent instability suggestive of in vivo lagging strand secondary structure.
description
1998 nî lūn-bûn
@nan
1998 թուականի Մայիսին հրատարակուած գիտական յօդուած
@hyw
1998 թվականի մայիսին հրատարակված գիտական հոդված
@hy
1998年の論文
@ja
1998年論文
@yue
1998年論文
@zh-hant
1998年論文
@zh-hk
1998年論文
@zh-mo
1998年論文
@zh-tw
1998年论文
@wuu
name
Cloned human FMR1 trinucleotid ...... ng strand secondary structure.
@ast
Cloned human FMR1 trinucleotid ...... ng strand secondary structure.
@en
Cloned human FMR1 trinucleotid ...... ng strand secondary structure.
@nl
type
label
Cloned human FMR1 trinucleotid ...... ng strand secondary structure.
@ast
Cloned human FMR1 trinucleotid ...... ng strand secondary structure.
@en
Cloned human FMR1 trinucleotid ...... ng strand secondary structure.
@nl
prefLabel
Cloned human FMR1 trinucleotid ...... ng strand secondary structure.
@ast
Cloned human FMR1 trinucleotid ...... ng strand secondary structure.
@en
Cloned human FMR1 trinucleotid ...... ng strand secondary structure.
@nl
P2860
P356
P1476
Cloned human FMR1 trinucleotid ...... ng strand secondary structure.
@en
P2093
P2860
P304
P356
10.1093/NAR/26.10.2353
P407
P577
1998-05-01T00:00:00Z