Triplet repeat RNA structure and its role as pathogenic agent and therapeutic target - Wikidata - awgldk - TriplyDB

Triplet repeat RNA structure and its role as pathogenic agent and therapeutic target

Triplet repeat RNA structure and its role as pathogenic agent and therapeutic target

http://www.wikidata.org/entity/Q35633648

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RAN translation and frameshifting as translational challenges at simple repeats of human neurodegenerative disorders Structural studies of CNG repeats Mouse models of polyglutamine diseases in therapeutic approaches: review and data table. Part II.Twisting right to left: A…A mismatch in a CAG trinucleotide repeat overexpansion provokes left-handed Z-DNA conformation A dynamic structural model of expanded RNA CAG repeats: a refined X-ray structure and computational investigations using molecular dynamics and umbrella sampling simulations.RNA phase transitions in repeat expansion disorders.Trinucleotide repeats: a structural perspective 'Costa da Morte' ataxia is spinocerebellar ataxia 36: clinical and genetic characterization.Examining the interactions of the splicing factor MBNL1 with target RNA sequences via a label-free, multiplex method Targeting toxic RNAs that cause myotonic dystrophy type 1 (DM1) with a bisamidinium inhibitor.Lomofungin and dilomofungin: inhibitors of MBNL1-CUG RNA binding with distinct cellular effects.Oligonucleotide-based strategies to combat polyglutamine diseases.An evaluation of oligonucleotide-based therapeutic strategies for polyQ diseases RNA-protein interactions in unstable microsatellite diseases.MBNL proteins and their target RNAs, interaction and splicing regulation.Barnacle: detecting and characterizing tandem duplications and fusions in transcriptome assemblies Effects on murine behavior and lifespan of selectively decreasing expression of mutant huntingtin allele by supt4h knockdown The role of the immune system in triplet repeat expansion diseases Huntingtin Exists as Multiple Splice Forms in Human Brain.RNA-binding protein misregulation in microsatellite expansion disorders RNA Structures as Mediators of Neurological Diseases and as Drug Targets.Nuclear retention of full-length HTT RNA is mediated by splicing factors MBNL1 and U2AF65 On the Applicability of Elastic Network Models for the Study of RNA CUG Trinucleotide Repeat Overexpansion.Identification of Plant-derived Alkaloids with Therapeutic Potential for Myotonic Dystrophy Type I RNA imaging in living cells - methods and applications.Cooperation meets competition in microRNA-mediated DMPK transcript regulation.Allele-selective inhibition of trinucleotide repeat genes.Mechanism of allele-selective inhibition of huntingtin expression by duplex RNAs that target CAG repeats: function through the RNAi pathway The first crystal structures of RNA-PNA duplexes and a PNA-PNA duplex containing mismatches--toward anti-sense therapy against TREDs RNA interference targeting CUG repeats in a mouse model of myotonic dystrophy.Structural characterization of a dimer of RNA duplexes composed of 8-bromoguanosine modified CGG trinucleotide repeats: a novel architecture of RNA quadruplexes A low absolute number of expanded transcripts is involved in myotonic dystrophy type 1 manifestation in muscle.RNA toxicity in polyglutamine disorders: concepts, models, and progress of research ss-siRNAs allele selectively inhibit ataxin-3 expression: multiple mechanisms for an alternative gene silencing strategy.Treatment of type 1 myotonic dystrophy by engineering site-specific RNA endonucleases that target (CUG)(n) repeats.RNA-binding proteins in microsatellite expansion disorders: mediators of RNA toxicity.Pre-mRNA splicing in disease and therapeutics.Treatment implications of C9ORF72.Emerging complexity of the HuD/ELAVl4 gene; implications for neuronal development, function, and dysfunction Small non-coding RNAs add complexity to the RNA pathogenic mechanisms in trinucleotide repeat expansion diseases.

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P2860

Triplet repeat RNA structure and its role as pathogenic agent and therapeutic target

http://www.wikidata.org/entity/Q35633648

description

2011 nî lūn-bûn

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2011年の論文

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2011年論文

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2011年論文

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2011年論文

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2011年論文

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2011年論文

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2011年论文

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2011年论文

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2011年论文

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name

Triplet repeat RNA structure and its role as pathogenic agent and therapeutic target

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Triplet repeat RNA structure and its role as pathogenic agent and therapeutic target

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type

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Triplet repeat RNA structure and its role as pathogenic agent and therapeutic target

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Triplet repeat RNA structure and its role as pathogenic agent and therapeutic target

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prefLabel

Triplet repeat RNA structure and its role as pathogenic agent and therapeutic target

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Triplet repeat RNA structure and its role as pathogenic agent and therapeutic target

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Triplet repeat RNA structure and its role as pathogenic agent and therapeutic target

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Agnieszka Mykowska

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Krzysztof Sobczak

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Marzena Wojciechowska

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Piotr Kozlowski

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Creative Commons Attribution-NonCommercial 3.0 Unported

P2860

Recruitment of human muscleblind proteins to (CUG)(n) expansions associated with myotonic dystrophy

Identification of a (CUG)n triplet repeat RNA-binding protein and its expression in myotonic dystrophy

Failure of MBNL1-dependent post-natal splicing transitions in myotonic dystrophy

Visualization of double-stranded RNAs from the myotonic dystrophy protein kinase gene and interactions with CUG-binding protein

In vivo co-localisation of MBNL protein with DMPK expanded-repeat transcripts

A natural antisense transcript at the Huntington's disease repeat locus regulates HTT expression

Hyperexpansion of GAA repeats affects post-initiation steps of FXN transcription in Friedreich's ataxia

HITS-CLIP yields genome-wide insights into brain alternative RNA processing

Correction of ClC-1 splicing eliminates chloride channelopathy and myotonia in mouse models of myotonic dystrophy

Facile FMR1 mRNA structure regulation by interruptions in CGG repeats

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10.1093/NAR/GKR729

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1

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Agnieszka Fiszer

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2012-01-01T00:00:00Z

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51639862

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21908410

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genetic variation

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3245940

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