Development of novel aminoglycoside (NB54) with reduced toxicity and enhanced suppression of disease-causing premature stop mutations - Wikidata - awgldk - TriplyDB

Development of novel aminoglycoside (NB54) with reduced toxicity and enhanced suppression of disease-causing premature stop mutations

Development of novel aminoglycoside (NB54) with reduced toxicity and enhanced suppression of disease-causing premature stop mutations

http://www.wikidata.org/entity/Q33704273

about

Molecular and cell-based therapies for muscle degenerations: a road under construction New developments in aminoglycoside therapy and ototoxicity New and emerging targeted therapies for cystic fibrosis New approaches to the treatment of orphan genetic disorders: Mitigating molecular pathologies using chemicals Identification of the molecular attributes required for aminoglycoside activity against Leishmania Cystic fibrosis transmembrane conductance regulator modulators in cystic fibrosis: current perspectives Evaluation of Aminoglycoside and Non-Aminoglycoside Compounds for Stop-Codon Readthrough Therapy in Four Lysosomal Storage Diseases Chemical-Induced Read-Through at Premature Termination Codons Determined by a Rapid Dual-Fluorescence System Based on S. cerevisiae Ex vivo treatment with a novel synthetic aminoglycoside NB54 in primary fibroblasts from Rett syndrome patients suppresses MECP2 nonsense mutations A model for neural development and treatment of Rett syndrome using human induced pluripotent stem cells Structural basis for selective targeting of leishmanial ribosomes: aminoglycoside derivatives as promising therapeutics.Assessment of nutrient supplement to reduce gentamicin-induced ototoxicity.Cisplatin and aminoglycoside antibiotics: hearing loss and its prevention.Aminoglycoside-stimulated readthrough of premature termination codons in selected genes involved in primary ciliary dyskinesia.The effect of gentamicin-induced readthrough on a novel premature termination codon of CD18 leukocyte adhesion deficiency patients.Synthetic aminoglycosides efficiently suppress cystic fibrosis transmembrane conductance regulator nonsense mutations and are enhanced by ivacaftor NBCe1 as a model carrier for understanding the structure-function properties of Na⁺ -coupled SLC4 transporters in health and disease.Aminoglycoside-Induced Premature Stop Codon Read-Through of Mucopolysaccharidosis Type I Patient Q70X and W402X Mutations in Cultured Cells.New trends in aminoglycosides use.Cystic fibrosis transmembrane conductance regulator protein repair as a therapeutic strategy in cystic fibrosis Translational read-through as an alternative approach for ocular gene therapy of retinal dystrophies caused by in-frame nonsense mutations.Design of a bioactive small molecule that targets the myotonic dystrophy type 1 RNA via an RNA motif-ligand database and chemical similarity searching.Pharmacologic management of Duchenne muscular dystrophy: target identification and preclinical trials Statistical analysis of readthrough levels for nonsense mutations in mammalian cells reveals a major determinant of response to gentamicin.Aminoglycoside-induced mutation suppression (stop codon readthrough) as a therapeutic strategy for Duchenne muscular dystrophy Increased selectivity toward cytoplasmic versus mitochondrial ribosome confers improved efficiency of synthetic aminoglycosides in fixing damaged genes: a strategy for treatment of genetic diseases caused by nonsense mutations Nonsense-mediated decay in genetic disease: friend or foe?Readthrough of nonsense mutations in Rett syndrome: evaluation of novel aminoglycosides and generation of a new mouse model Analysis of carbohydrates and glycoconjugates by matrix-assisted laser desorption/ionization mass spectrometry: an update for 2009-2010.Post-transcriptionally regulated expression system in human xenogeneic transplantation models.Suppression of nonsense mutations as a therapeutic approach to treat genetic diseases.Suppression of CFTR premature termination codons and rescue of CFTR protein and function by the synthetic aminoglycoside NB54 The designer aminoglycoside NB84 significantly reduces glycosaminoglycan accumulation associated with MPS I-H in the Idua-W392X mouse.Current understanding of usher syndrome type II.Expanding rare disease drug trials based on shared molecular etiology Dysferlin and animal models for dysferlinopathy USH1G with unique retinal findings caused by a novel truncating mutation identified by genome-wide linkage analysis.Suppression of premature termination codons as a therapeutic approach.Synthesis and Biological Activity of Mono- and Di-N-acylated Aminoglycosides.A comparative evaluation of NB30, NB54 and PTC124 in translational read-through efficacy for treatment of an USH1C nonsense mutation

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P2860

Development of novel aminoglycoside (NB54) with reduced toxicity and enhanced suppression of disease-causing premature stop mutations

http://www.wikidata.org/entity/Q33704273

description

2009 nî lūn-bûn

@nan

2009 թուականի Մայիսին հրատարակուած գիտական յօդուած

@hyw

2009 թվականի մայիսին հրատարակված գիտական հոդված

@hy

2009年の論文

@ja

2009年論文

@yue

2009年論文

@zh-hant

2009年論文

@zh-hk

2009年論文

@zh-mo

2009年論文

@zh-tw

2009年论文

@wuu

name

Development of novel aminoglyc ...... using premature stop mutations

@ast

Development of novel aminoglyc ...... using premature stop mutations

@en

type

label

Development of novel aminoglyc ...... using premature stop mutations

@ast

Development of novel aminoglyc ...... using premature stop mutations

@en

prefLabel

Development of novel aminoglyc ...... using premature stop mutations

@ast

Development of novel aminoglyc ...... using premature stop mutations

@en

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P1433

Journal of Medicinal Chemistry

P1476

Development of novel aminoglyc ...... using premature stop mutations

@en

P2093

Annie Rebibo-Sabbah

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

Daniel S Pilch

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

Fuquan Chen

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

Igor Nudelman

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

Jochen Schacht

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

Mariana Hainrichson

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

Marina Cherniavsky

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

Tamar Ben-Yosef

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

Timor Baasov

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

Valery Belakhov

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

P2860

Five Percent of Normal Cystic Fibrosis Transmembrane Conductance Regulator mRNA Ameliorates the Severity of Pulmonary Disease in Cystic Fibrosis

The complex of a designer antibiotic with a model aminoacyl site of the 30S ribosomal subunit revealed by X-ray crystallography

Differential selectivity of natural and synthetic aminoglycosides towards the eukaryotic and prokaryotic decoding A sites

The bacterial and mitochondrial ribosomal A-site molecular switches possess different conformational substates

Aspirin to prevent gentamicin-induced hearing loss

Correction of genetic disease by making sense from nonsense.

Aminoglycoside antibiotics.

Aminoglycoside antibiotics restore dystrophin function to skeletal muscles of mdx mice

Gentamicin-induced correction of CFTR function in patients with cystic fibrosis and CFTR stop mutations.

Aminoglycoside antibiotics mediate context-dependent suppression of termination codons in a mammalian translation system

P304

2836-2845

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scholarly article

P356

10.1021/JM801640K

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P407

P433

9

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P478

52

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P577

2009-05-01T00:00:00Z

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P5875

24222350

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P698

19309154

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P932

2832307

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