Partners in crime: bidirectional transcription in unstable microsatellite disease. - Wikidata - awgldk - TriplyDB

Partners in crime: bidirectional transcription in unstable microsatellite disease.

Partners in crime: bidirectional transcription in unstable microsatellite disease.

http://www.wikidata.org/entity/Q37724514

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A natural antisense transcript at the Huntington's disease repeat locus regulates HTT expression New insights into repeat instability: role of RNA•DNA hybrids RAN translation and frameshifting as translational challenges at simple repeats of human neurodegenerative disorders Involvement of long noncoding RNAs in diseases affecting the central nervous system Triplet repeat-derived siRNAs enhance RNA-mediated toxicity in a Drosophila model for myotonic dystrophy 5meCpG epigenetic marks neighboring a primate-conserved core promoter short tandem repeat indicate X-chromosome inactivation Developing informative microsatellite makers for non-model species using reference mapping against a model species' genome Processing of double-R-loops in (CAG)·(CTG) and C9orf72 (GGGGCC)·(GGCCCC) repeats causes instability.CTCF regulates ataxin-7 expression through promotion of a convergently transcribed, antisense noncoding RNA.Repeat associated non-ATG translation initiation: one DNA, two transcripts, seven reading frames, potentially nine toxic entities!RNA-protein interactions in unstable microsatellite diseases.Ubiquitous expression of CUG or CAG trinucleotide repeat RNA causes common morphological defects in a Drosophila model of RNA-mediated pathology Non-ATG-initiated translation directed by microsatellite expansions.Repeat associated non-ATG (RAN) translation: new starts in microsatellite expansion disorders.Trinucleotide expansion in disease: why is there a length threshold?Determinants of R-loop formation at convergent bidirectionally transcribed trinucleotide repeats Triplet repeat RNA structure and its role as pathogenic agent and therapeutic target RNA-binding protein misregulation in microsatellite expansion disorders Chromatin changes in the development and pathology of the Fragile X-associated disorders and Friedreich ataxia.The disease-associated r(GGGGCC)n repeat from the C9orf72 gene forms tract length-dependent uni- and multimolecular RNA G-quadruplex structures The Enemy within: Innate Surveillance-Mediated Cell Death, the Common Mechanism of Neurodegenerative Disease.Bidirectional transcription of trinucleotide repeats: roles for excision repair.Evidence relevant to untargeted and transgenerational effects in the offspring of irradiated parents RNA pathogenesis via Toll-like receptor-activated inflammation in expanded repeat neurodegenerative diseases.Regulation of chromatin structure by long noncoding RNAs: focus on natural antisense transcripts Repeat-associated non-ATG (RAN) translation in neurological disease.Targeted degradation of sense and antisense C9orf72 RNA foci as therapy for ALS and frontotemporal degeneration.Consensus paper: pathological mechanisms underlying neurodegeneration in spinocerebellar ataxias.Most expression and splicing changes in myotonic dystrophy type 1 and type 2 skeletal muscle are shared with other muscular dystrophies.Mechanisms of toxicity in C9FTLD/ALS.Structural Characteristics of Simple RNA Repeats Associated with Disease and their Deleterious Protein Interactions.Cellular toxicity of expanded RNA repeats: focus on RNA foci.RNA-binding proteins in microsatellite expansion disorders: mediators of RNA toxicity.Small non-coding RNAs add complexity to the RNA pathogenic mechanisms in trinucleotide repeat expansion diseases.Brain pathology in myotonic dystrophy: when tauopathy meets spliceopathy and RNAopathy.Transcription-induced DNA toxicity at trinucleotide repeats: double bubble is trouble.Elimination of Toxic Microsatellite Repeat Expansion RNA by RNA-Targeting Cas9.RNA toxicity induced by expanded CAG repeats in Huntington's disease.R Loops and Links to Human Disease.The role of RNA metabolism in neurological diseases.

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Partners in crime: bidirectional transcription in unstable microsatellite disease.

http://www.wikidata.org/entity/Q37724514

description

article científic

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article scientifique

@fr

articolo scientifico

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artigo científico

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bilimsel makale

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scientific article published on 04 April 2010

@en

vedecký článok

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vetenskaplig artikel

@sv

videnskabelig artikel

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vědecký článek

@cs

name

Partners in crime: bidirectional transcription in unstable microsatellite disease.

@en

Partners in crime: bidirectional transcription in unstable microsatellite disease.

@nl

type

label

Partners in crime: bidirectional transcription in unstable microsatellite disease.

@en

Partners in crime: bidirectional transcription in unstable microsatellite disease.

@nl

prefLabel

Partners in crime: bidirectional transcription in unstable microsatellite disease.

@en

Partners in crime: bidirectional transcription in unstable microsatellite disease.

@nl

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Human Molecular Genetics

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Partners in crime: bidirectional transcription in unstable microsatellite disease.

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Konstantinos Charizanis

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

Maurice S Swanson

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Ranjan Batra

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

P2860

A novel RNA transcript with antiapoptotic function is silenced in fragile X syndrome

The SCA8 transcript is an antisense RNA to a brain-specific transcript encoding a novel actin-binding protein (KLHL1)

Pathogenic mechanisms of a polyglutamine-mediated neurodegenerative disease, spinocerebellar ataxia type 1

A fragile balance: FMR1 expression levels

In search of antisense

Identification of a gene (FMR-1) containing a CGG repeat coincident with a breakpoint cluster region exhibiting length variation in fragile X syndrome

Puralpha is essential for postnatal brain development and developmentally coupled cellular proliferation as revealed by genetic inactivation in the mouse

Trinucleotide Repeat Disorders

RNA and disease

Non-coding RNAs: regulators of disease

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R77-82

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scholarly article

P356

10.1093/HMG/DDQ132

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R1

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19

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2010-04-04T00:00:00Z

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20368264

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