Structural analysis of slipped-strand DNA (S-DNA) formed in (CTG)n. (CAG)n repeats from the myotonic dystrophy locus. - Wikidata - wikimedia - TriplyDB

Structural analysis of slipped-strand DNA (S-DNA) formed in (CTG)n. (CAG)n repeats from the myotonic dystrophy locus.

Structural analysis of slipped-strand DNA (S-DNA) formed in (CTG)n. (CAG)n repeats from the myotonic dystrophy locus.

http://www.wikidata.org/entity/Q39722798

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Molecular basis for expression of common and rare fragile sites Mapping of an origin of DNA replication in the promoter of fragile X gene FMR1 Multi-species sequence comparison reveals dynamic evolution of the elastin gene that has involved purifying selection and lineage-specific insertions/deletions Structural roles of CTG repeats in slippage expansion during DNA replication Mechanistic features of CAG*CTG repeat contractions in cultured cells revealed by a novel genetic assay Length-dependent energetics of (CTG)n and (CAG)n trinucleotide repeats.Role of LrpC from Bacillus subtilis in DNA transactions during DNA repair and recombination.DNA triplet repeat expansion and mismatch repair The novel double-folded structure of d(GCATGCATGC): a possible model for triplet-repeat sequences DNA polymorphism in crystals: three stable conformations for the decadeoxynucleotide d(GCATGCATGC)Unusual structures are present in DNA fragments containing super-long Huntingtin CAG repeats DNA Replication Dynamics of the GGGGCC Repeat of the C9orf72 Gene.Processing of double-R-loops in (CAG)·(CTG) and C9orf72 (GGGGCC)·(GGCCCC) repeats causes instability.Isolated short CTG/CAG DNA slip-outs are repaired efficiently by hMutSbeta, but clustered slip-outs are poorly repaired.Stoichiometry of base excision repair proteins correlates with increased somatic CAG instability in striatum over cerebellum in Huntington's disease transgenic mice Inheritance patterns of ATCCT repeat interruptions in spinocerebellar ataxia type 10 (SCA10) expansions Rapid, high fidelity analysis of simple sequence repeats on an electronically active DNA microchip.Topoisomerase 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.Conformational energetics of stable and metastable states formed by DNA triplet repeat oligonucleotides: implications for triplet expansion diseases Determinants of R-loop formation at convergent bidirectionally transcribed trinucleotide repeats Structure of even/odd trinucleotide repeat sequences modulates persistence of non-B conformations and conversion to duplex Detection of slipped-DNAs at the trinucleotide repeats of the myotonic dystrophy type I disease locus in patient tissues.Global structure of a DNA three-way junction by solution NMR: towards prediction of 3H fold Trinucleotide repeat DNA alters structure to minimize the thermodynamic impact of 8-oxo-7,8-dihydroguanine.Repeat instability during DNA repair: Insights from model systems Altered replication in human cells promotes DMPK (CTG)(n) · (CAG)(n) repeat instability Triptycene-based small molecules modulate (CAG)·(CTG) repeat junctions.Human mismatch repair protein hMutLα is required to repair short slipped-DNAs of trinucleotide repeats.Oligodeoxynucleotide binding to (CTG) · (CAG) microsatellite repeats inhibits replication fork stalling, hairpin formation, and genome instability.Interconverting conformations of slipped-DNA junctions formed by trinucleotide repeats affect repair outcome Role of DNA secondary structures in fragile site breakage along human chromosome 10 A Z-DNA sequence reduces slipped-strand structure formation in the myotonic dystrophy type 2 (CCTG) x (CAGG) repeat Inhibition of DNA synthesis facilitates expansion of low-complexity repeats: is strand slippage stimulated by transient local depletion of specific dNTPs?Absence of MutSβ leads to the formation of slipped-DNA for CTG/CAG contractions at primate replication forks.Transcription influences the types of deletion and expansion products in an orientation-dependent manner from GAC*GTC repeats A brief history of triplet repeat diseases.Abnormal base excision repair at trinucleotide repeats associated with diseases: a tissue-selective mechanism.DNA ligase I competes with FEN1 to expand repetitive DNA sequences in vitro.Transcription-induced DNA toxicity at trinucleotide repeats: double bubble is trouble.

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P2860

Structural analysis of slipped-strand DNA (S-DNA) formed in (CTG)n. (CAG)n repeats from the myotonic dystrophy locus.

http://www.wikidata.org/entity/Q39722798

description

1998 nî lūn-bûn

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1998年の論文

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1998年論文

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1998年論文

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1998年論文

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1998年論文

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1998年論文

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1998年论文

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1998年论文

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1998年论文

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name

Structural analysis of slipped ...... the myotonic dystrophy locus.

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Structural analysis of slipped-strand DNA

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type

label

Structural analysis of slipped ...... the myotonic dystrophy locus.

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Structural analysis of slipped-strand DNA

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Structural analysis of slipped ...... the myotonic dystrophy locus.

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Structural analysis of slipped-strand DNA

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Nucleic Acids Research

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Structural analysis of slipped ...... the myotonic dystrophy locus.

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C E Pearson

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

J D Griffith

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R R Sinden

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Y H Wang

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P2860

Genetically unstable CXG repeats are structurally dynamic and have a high propensity for folding. An NMR and UV spectroscopic study

Myotonic dystrophy mutation: an unstable CTG repeat in the 3' untranslated region of the gene

Identification of mismatch repair genes and their role in the development of cancer

Trinucleotide repeats that expand in human disease form hairpin structures in vitro

Intramolecular DNA triplexes in supercoiled plasmids.

Kinking of DNA and RNA by base bulges.

Deletions of bases in one strand of duplex DNA, in contrast to single-base mismatches, produce highly kinked molecules: possible relevance to the folding of single-stranded nucleic acids.

Structure and dynamics of the DNA hairpins formed by tandemly repeated CTG triplets associated with myotonic dystrophy.

Stability of intrastrand hairpin structures formed by the CAG/CTG class of DNA triplet repeats associated with neurological diseases.

Dynamic mutations: a new class of mutations causing human disease.

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3

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