Rationally designed small molecules targeting the RNA that causes myotonic dystrophy type 1 are potently bioactive. - Wikidata - awgldk - TriplyDB

Rationally designed small molecules targeting the RNA that causes myotonic dystrophy type 1 are potently bioactive.

Rationally designed small molecules targeting the RNA that causes myotonic dystrophy type 1 are potently bioactive.

http://www.wikidata.org/entity/Q34158462

about

Myotonic dystrophy: is a narrow focus obscuring the rest of the field?Structure based approaches for targeting non-coding RNAs with small molecules The unstable repeats--three evolving faces of neurological disease Design of a bioactive small molecule that targets r(AUUCU) repeats in spinocerebellar ataxia 10 Small Molecule Inhibition of miR-544 Biogenesis Disrupts Adaptive Responses to Hypoxia by Modulating ATM-mTOR Signaling Approaches to Validate and Manipulate RNA Targets with Small Molecules in Cells Characterization and in vitro activity of a branched peptide boronic acid that interacts with HIV-1 RRE RNA TWEAK/Fn14, a pathway and novel therapeutic target in myotonic dystrophy.Biological Efficacy and Toxicity of Diamidines in Myotonic Dystrophy Type 1 Models.Single-molecule study of the CUG repeat-MBNL1 interaction and its inhibition by small molecules.Computational investigation of RNA CUG repeats responsible for myotonic dystrophy 1 Methods to enable the design of bioactive small molecules targeting RNA.Two-dimensional combinatorial screening enables the bottom-up design of a microRNA-10b inhibitor Lomofungin and dilomofungin: inhibitors of MBNL1-CUG RNA binding with distinct cellular effects.Aryl-substituted aminobenzimidazoles targeting the hepatitis C virus internal ribosome entry site.Reducing levels of toxic RNA with small molecules MBNL proteins and their target RNAs, interaction and splicing regulation.A small molecule that targets r(CGG)(exp) and improves defects in fragile X-associated tremor ataxia syndrome.Probing a 2-aminobenzimidazole library for binding to RNA internal loops via two-dimensional combinatorial screening.Modifications to toxic CUG RNAs induce structural stability, rescue mis-splicing in a myotonic dystrophy cell model and reduce toxicity in a myotonic dystrophy zebrafish model.Defining RNA motif-aminoglycoside interactions via two-dimensional combinatorial screening and structure-activity relationships through sequencing.Induction and reversal of myotonic dystrophy type 1 pre-mRNA splicing defects by small molecules.Targeting the r(CGG) repeats that cause FXTAS with modularly assembled small molecules and oligonucleotides Features of modularly assembled compounds that impart bioactivity against an RNA target.Aberrant RNA homeostasis in amyotrophic lateral sclerosis: potential for new therapeutic targets?Developing bivalent ligands to target CUG triplet repeats, the causative agent of myotonic dystrophy type 1.Small molecules that target the toxic RNA in myotonic dystrophy type 2.Sequence-based design of bioactive small molecules that target precursor microRNAs.HIV-1 drug discovery: targeting folded RNA structures with branched peptides.RNA Structures as Mediators of Neurological Diseases and as Drug Targets.Identification of Plant-derived Alkaloids with Therapeutic Potential for Myotonic Dystrophy Type I Precise small-molecule recognition of a toxic CUG RNA repeat expansion.In silico discovery of substituted pyrido[2,3-d]pyrimidines and pentamidine-like compounds with biological activity in myotonic dystrophy models.Rational design of bioactive, modularly assembled aminoglycosides targeting the RNA that causes myotonic dystrophy type 1.Antisense oligonucleotides: rising stars in eliminating RNA toxicity in myotonic dystrophy.Small-molecule-mediated cleavage of RNA in living cells.Inforna 2.0: A Platform for the Sequence-Based Design of Small Molecules Targeting Structured RNAs Rational design of chemical genetic probes of RNA function and lead therapeutics targeting repeating transcripts.Influence of dimethylsulfoxide on RNA structure and ligand binding.Covalent small-molecule-RNA complex formation enables cellular profiling of small-molecule-RNA interactions

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Rationally designed small molecules targeting the RNA that causes myotonic dystrophy type 1 are potently bioactive.

http://www.wikidata.org/entity/Q34158462

description

2012 nî lūn-bûn

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2012 թուականի Մարտին հրատարակուած գիտական յօդուած

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2012 թվականի մարտին հրատարակված գիտական հոդված

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2012年の論文

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2012年論文

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2012年論文

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name

Rationally designed small mole ...... type 1 are potently bioactive.

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Rationally designed small mole ...... type 1 are potently bioactive.

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Rationally designed small mole ...... type 1 are potently bioactive.

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type

label

Rationally designed small mole ...... type 1 are potently bioactive.

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Rationally designed small mole ...... type 1 are potently bioactive.

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Rationally designed small mole ...... type 1 are potently bioactive.

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prefLabel

Rationally designed small mole ...... type 1 are potently bioactive.

@ast

Rationally designed small mole ...... type 1 are potently bioactive.

@en

Rationally designed small mole ...... type 1 are potently bioactive.

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ACS Chemical Biology

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Rationally designed small mole ...... type 1 are potently bioactive.

@en

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Charles A Thornton

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

Jessica L Childs-Disney

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

Matthew D Disney

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

Suzanne G Rzuczek

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Initial sequencing and analysis of the human genome

The Sequence of the Human Genome

Muscleblind proteins regulate alternative splicing

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

RNA CUG repeats sequester CUGBP1 and alter protein levels and activity of CUGBP1

Colocalization of muscleblind with RNA foci is separable from mis-regulation of alternative splicing in myotonic dystrophy

A muscleblind knockout model for myotonic dystrophy

Woodchuck post-transcriptional element induces nuclear export of myotonic dystrophy 3' untranslated region transcripts.

An antisense-based functional genomics approach for identification of genes critical for growth of Candida albicans.

High-efficiency FLP and PhiC31 site-specific recombination in mammalian cells.

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856-862

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scholarly article

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10.1021/CB200408A

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5

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7

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221831082

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22332923

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3356481

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