Slipped-strand DNAs formed by long (CAG)*(CTG) repeats: slipped-out repeats and slip-out junctions. - Wikidata - wikimedia - TriplyDB

Slipped-strand DNAs formed by long (CAG)*(CTG) repeats: slipped-out repeats and slip-out junctions.

Slipped-strand DNAs formed by long (CAG)*(CTG) repeats: slipped-out repeats and slip-out junctions.

http://www.wikidata.org/entity/Q39687235

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DNA slip-outs cause RNA polymerase II arrest in vitro: potential implications for genetic instability Comparative genomics and molecular dynamics of DNA repeats in eukaryotes 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.Advances in mechanisms of genetic instability related to hereditary neurological diseases.Continuous and periodic expansion of CAG repeats in Huntington's disease R6/1 mice Modeling diseases of noncoding unstable repeat expansions using mutant pluripotent stem cells.Unusual structures are present in DNA fragments containing super-long Huntingtin CAG repeats Incision-dependent and error-free repair of (CAG)(n)/(CTG)(n) hairpins in human cell extracts Isolated short CTG/CAG DNA slip-outs are repaired efficiently by hMutSbeta, but clustered slip-outs are poorly repaired.MSH2 ATPase domain mutation affects CTG*CAG repeat instability in transgenic mice.R loops stimulate genetic instability of CTG.CAG repeats.Replication inhibitors modulate instability of an expanded trinucleotide repeat at the myotonic dystrophy type 1 disease locus in human cells.Intergenerational instability of the expanded CTG repeat in the DMPK gene: studies in human gametes and preimplantation embryos.NuA4 initiates dynamic histone H4 acetylation to promote high-fidelity sister chromatid recombination at postreplication gaps.Non-B DNA structure-induced genetic instability and evolution.Sequence length dictates repeated CAG folding in three-way junctions 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 CTG repeat instability and size variation timing in DNA repair-deficient mice.Microsatellite repeat instability and neurological disease.Detection of slipped-DNAs at the trinucleotide repeats of the myotonic dystrophy type I disease locus in patient tissues.TSSV: a tool for characterization of complex allelic variants in pure and mixed genomes.Global structure of a DNA three-way junction by solution NMR: towards prediction of 3H fold Incidence and persistence of 8-oxo-7,8-dihydroguanine within a hairpin intermediate exacerbates a toxic oxidation cycle associated with trinucleotide repeat expansion Purification, crystallization and preliminary X-ray diffraction analysis of the human mismatch repair protein MutSβ Premutation huntingtin allele adopts a non-B conformation and contains a hot spot for DNA damage.Trinucleotide repeat DNA alters structure to minimize the thermodynamic impact of 8-oxo-7,8-dihydroguanine.Biochemical studies of the Saccharomyces cerevisiae Mph1 helicase on junction-containing DNA structures Triptycene-based small molecules modulate (CAG)·(CTG) repeat junctions.In vitro repair of DNA hairpins containing various numbers of CAG/CTG trinucleotide repeats.The Werner syndrome protein promotes CAG/CTG repeat stability by resolving large (CAG)(n)/(CTG)(n) hairpins 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 Coordinated processing of 3' slipped (CAG)n/(CTG)n hairpins by DNA polymerases β and δ preferentially induces repeat expansions.Extrahelical (CAG)/(CTG) triplet repeat elements support proliferating cell nuclear antigen loading and MutLα endonuclease activation A Z-DNA sequence reduces slipped-strand structure formation in the myotonic dystrophy type 2 (CCTG) x (CAGG) repeat FMR1: a gene with three faces.Mismatch recognition protein MutSbeta does not hijack (CAG)n hairpin repair in vitro.Circular dichroism and conformational polymorphism of DNA.

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Slipped-strand DNAs formed by long (CAG)*(CTG) repeats: slipped-out repeats and slip-out junctions.

http://www.wikidata.org/entity/Q39687235

description

2002 nî lūn-bûn

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Slipped-strand DNAs formed by long

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Slipped-strand DNAs formed by ...... epeats and slip-out junctions.

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Slipped-strand DNAs formed by long

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Slipped-strand DNAs formed by ...... epeats and slip-out junctions.

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Nucleic Acids Research

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Slipped-strand DNAs formed by ...... epeats and slip-out junctions.

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Arvin C Dar

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Christopher E Pearson

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John D Cleary

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Kerrie Nichol

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Mandy Tam

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S Erin Montgomery

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Yuh-Hwa Wang

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P2860

Structures of helical junctions in nucleic acids

Molecular basis of genetic instability of triplet repeats

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

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

Dramatic mutation instability in HD mouse striatum: does polyglutamine load contribute to cell-specific vulnerability in Huntington's disease?

The intrinsically unstable life of DNA triplet repeats associated with human hereditary disorders.

DNA secondary structure: a common and causative factor for expansion in human disease.

Fourteen and counting: unraveling trinucleotide repeat diseases.

The junction-resolving enzymes.

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

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10.1093/NAR/GKF572

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20

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30

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12384601

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137136

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