Triplet repeat expansion in myotonic dystrophy alters the adjacent chromatin structure. - Wikidata - wikimedia - TriplyDB

Triplet repeat expansion in myotonic dystrophy alters the adjacent chromatin structure.

Triplet repeat expansion in myotonic dystrophy alters the adjacent chromatin structure.

http://www.wikidata.org/entity/Q34226936

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Recruitment of human muscleblind proteins to (CUG)(n) expansions associated with myotonic dystrophy Functional analysis of the homeodomain protein SIX5.Epigenetics and Triplet-Repeat Neurological Diseases DNA triplet repeat expansion and mismatch repair Epigenetic boundaries of tumour suppressor gene promoters: the CTCF connection and its role in carcinogenesis Heterozygous loss of Six5 in mice is sufficient to cause ocular cataracts Molecular cloning and characterization of a novel mouse macrophage gene that encodes a nuclear protein comprising polyglutamine repeats and interspersing histidines Cytoplasmic CUG RNA foci are insufficient to elicit key DM1 features.High frequency of microsatellites in S. cerevisiae meiotic recombination hotspots Spinocerebellar ataxia type 8 larger triplet expansion alters histone modification and induces RNA foci.The impact of local genome sequence on defining heterochromatin domains.Altered telomere nuclear matrix interactions and nucleosomal periodicity in ataxia telangiectasia cells before and after ionizing radiation treatment The role of MOF in the ionizing radiation response is conserved in Drosophila melanogaster Expanded CTG repeat demarcates a boundary for abnormal CpG methylation in myotonic dystrophy patient tissues Myotonic dystrophy: molecular windows on a complex etiology.Molecular parameters of hyperthermia for radiosensitization.RNA steady-state defects in myotonic dystrophy are linked to nuclear exclusion of SHARP.Epigenetic mechanisms and genome stability.Repeat-mediated epigenetic dysregulation of the FMR1 gene in the fragile X-related disorders.Myotonic dystrophy: RNA pathogenesis comes into focus.Instability of (CTG)n•(CAG)n trinucleotide repeats and DNA synthesis Repeat instability: mechanisms of dynamic mutations.CAG/CTG repeats alter the affinity for the histone core and the positioning of DNA in the nucleosome.Alternative splicing and muscular dystrophy.Misregulation of alternative splicing causes pathogenesis in myotonic dystrophy.Transcriptional abnormality in myotonic dystrophy affects DMPK but not neighboring genes Instability and chromatin structure of expanded trinucleotide repeats Dnmt1 deficiency promotes CAG repeat expansion in the mouse germline Bidirectional transcription of trinucleotide repeats: roles for excision repair.Chromatin remodeling in the noncoding repeat expansion diseases.The biological effects of simple tandem repeats: lessons from the repeat expansion diseases.RNA metabolism in myotonic dystrophy: patient muscle shows decreased insulin receptor RNA and protein consistent with abnormal insulin resistance.The [(G/C)3NN]n motif: a common DNA repeat that excludes nucleosomes.Telomeres, histone code, and DNA damage response.Pathogenic mechanisms of myotonic dystrophy Transcriptionally Repressive Chromatin Remodelling and CpG Methylation in the Presence of Expanded CTG-Repeats at the DM1 Locus.Microsatellite spreading in the human genome: evolutionary mechanisms and structural implications.Epigenetic changes and non-coding expanded repeats.Partners in crime: bidirectional transcription in unstable microsatellite disease.The yin and yang of repair mechanisms in DNA structure-induced genetic instability.

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P2860

Triplet repeat expansion in myotonic dystrophy alters the adjacent chromatin structure.

http://www.wikidata.org/entity/Q34226936

description

1995 nî lūn-bûn

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1995 թուականի Յունիսին հրատարակուած գիտական յօդուած

@hyw

1995 թվականի հունիսին հրատարակված գիտական հոդված

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1995年の論文

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1995年論文

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1995年論文

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1995年論文

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1995年論文

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1995年論文

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1995年论文

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name

Triplet repeat expansion in myotonic dystrophy alters the adjacent chromatin structure.

@ast

Triplet repeat expansion in myotonic dystrophy alters the adjacent chromatin structure.

@en

Triplet repeat expansion in myotonic dystrophy alters the adjacent chromatin structure.

@nl

type

label

Triplet repeat expansion in myotonic dystrophy alters the adjacent chromatin structure.

@ast

Triplet repeat expansion in myotonic dystrophy alters the adjacent chromatin structure.

@en

Triplet repeat expansion in myotonic dystrophy alters the adjacent chromatin structure.

@nl

prefLabel

Triplet repeat expansion in myotonic dystrophy alters the adjacent chromatin structure.

@ast

Triplet repeat expansion in myotonic dystrophy alters the adjacent chromatin structure.

@en

Triplet repeat expansion in myotonic dystrophy alters the adjacent chromatin structure.

@nl

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PNAS.92.12.5465

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Proceedings of the National Academy of Sciences of the United States of America

P1476

Triplet repeat expansion in myotonic dystrophy alters the adjacent chromatin structure.

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Otten AD

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

Tapscott SJ

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P2860

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

Differences and similarities in DNA-binding preferences of MyoD and E2A protein complexes revealed by binding site selection

Minimal expression of myotonic dystrophy: a clinical and molecular analysis.

The correlation of age of onset with CTG trinucleotide repeat amplification in myotonic dystrophy.

A study of DNA methylation in myotonic dystrophy.

French myotonic dystrophy families show expansion of a CTG repeat in complete linkage disequilibrium with an intragenic 1 kb insertion

Molecular basis of myotonic dystrophy: expansion of a trinucleotide (CTG) repeat at the 3' end of a transcript encoding a protein kinase family member.

Characterization of the myotonic dystrophy region predicts multiple protein isoform-encoding mRNAs.

Activation of muscle-specific genes in pigment, nerve, fat, liver, and fibroblast cell lines by forced expression of MyoD.

Trans-inactivation of the Drosophila brown gene: evidence for transcriptional repression and somatic pairing dependence.

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