Two new pimelic diphenylamide HDAC inhibitors induce sustained frataxin upregulation in cells from Friedreich's ataxia patients and in a mouse model - Wikidata - awgldk - TriplyDB

Two new pimelic diphenylamide HDAC inhibitors induce sustained frataxin upregulation in cells from Friedreich's ataxia patients and in a mouse model

Two new pimelic diphenylamide HDAC inhibitors induce sustained frataxin upregulation in cells from Friedreich's ataxia patients and in a mouse model

http://www.wikidata.org/entity/Q28472583

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Epigenetics and Triplet-Repeat Neurological Diseases Small molecule inhibitors of zinc-dependent histone deacetylases The promise and perils of HDAC inhibitors in neurodegeneration Pharmacological screening using an FXN-EGFP cellular genomic reporter assay for the therapy of Friedreich ataxia Development of frataxin gene expression measures for the evaluation of experimental treatments in Friedreich's ataxia Silencing of Fem1cR3 gene expression in the DBA/2J mouse precedes retinal ganglion cell death and is associated with histone deacetylase activity Inhibition of histone deacetylase 3 causes replication stress in cutaneous T cell lymphoma Lymphoblast Oxidative Stress Genes as Potential Biomarkers of Disease Severity and Drug Effect in Friedreich's Ataxia Disruption of Higher Order DNA Structures in Friedreich's Ataxia (GAA)n Repeats by PNA or LNA Targeting Prolonged treatment with pimelic o-aminobenzamide HDAC inhibitors ameliorates the disease phenotype of a Friedreich ataxia mouse model Mesenchymal stem cells restore frataxin expression and increase hydrogen peroxide scavenging enzymes in Friedreich ataxia fibroblasts HDAC3 is a critical negative regulator of long-term memory formation.HDAC3-selective inhibitor enhances extinction of cocaine-seeking behavior in a persistent manner.Novel frataxin isoforms may contribute to the pathological mechanism of Friedreich ataxia Quantitative proteomic analysis identifies targets and pathways of a 2-aminobenzamide HDAC inhibitor in Friedreich's ataxia patient iPSC-derived neural stem cells.Repeat expansion affects both transcription initiation and elongation in friedreich ataxia cells A GAA repeat expansion reporter model of Friedreich's ataxia recapitulates the genomic context and allows rapid screening of therapeutic compounds.Kinetically Selective Inhibitors of Histone Deacetylase 2 (HDAC2) as Cognition Enhancers A novel GAA-repeat-expansion-based mouse model of Friedreich's ataxia Mechanism of Action of 2-Aminobenzamide HDAC Inhibitors in Reversing Gene Silencing in Friedreich's Ataxia.Epigenetic therapy for Friedreich ataxia Bromodomain inhibitors regulate the C9ORF72 locus in ALS Inhibition of class I histone deacetylase activity represses matrix metalloproteinase-2 and -9 expression and preserves LV function postmyocardial infarction.Epigenetics, epidemiology and mitochondrial DNA diseases.Chromatin changes in the development and pathology of the Fragile X-associated disorders and Friedreich ataxia.A role for epigenetic changes in the development of retinal neurodegenerative conditions.DNA mismatch repair complex MutSβ promotes GAA·TTC repeat expansion in human cells Evidence for chromosome fragility at the frataxin locus in Friedreich ataxia.Why Hydroxamates May Not Be the Best Histone Deacetylase Inhibitors--What Some May Have Forgotten or Would Rather Forget?Epigenetics in Friedreich's Ataxia: Challenges and Opportunities for Therapy.A gene expression phenotype in lymphocytes from Friedreich ataxia patients.HDAC 3-selective inhibitor RGFP966 demonstrates anti-inflammatory properties in RAW 264.7 macrophages and mouse precision-cut lung slices by attenuating NF-κB p65 transcriptional activity.Epigenetics in nucleotide repeat expansion disorders.Genes and epigenetic processes as prospective pain targets Reversal of epigenetic promoter silencing in Friedreich ataxia by a class I histone deacetylase inhibitor.Rationale for the development of 2-aminobenzamide histone deacetylase inhibitors as therapeutics for Friedreich ataxia.Increasing frataxin gene expression with histone deacetylase inhibitors as a therapeutic approach for Friedreich's ataxia.Photoreactive "nanorulers" detect a novel conformation of full length HDAC3-SMRT complex in solution Consensus paper: pathological mechanisms underlying neurodegeneration in spinocerebellar ataxias.Current and emerging treatment options in the management of Friedreich ataxia.

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P2860

Two new pimelic diphenylamide HDAC inhibitors induce sustained frataxin upregulation in cells from Friedreich's ataxia patients and in a mouse model

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description

2010 nî lūn-bûn

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2010 թուականի Յունուարին հրատարակուած գիտական յօդուած

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2010 թվականի հունվարին հրատարակված գիտական հոդված

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2010年の論文

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Two new pimelic diphenylamide ...... patients and in a mouse model

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Two new pimelic diphenylamide ...... patients and in a mouse model

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C James Chou

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Elisabetta Soragni

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Glenn Barnes

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James R Rusche

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P2860

HDAC inhibitors correct frataxin deficiency in a Friedreich ataxia mouse model

Frataxin is reduced in Friedreich ataxia patients and is associated with mitochondrial membranes

Rb interacts with histone deacetylase to repress transcription

FDA approval summary: vorinostat for treatment of advanced primary cutaneous T-cell lymphoma.

Chemical probes identify a role for histone deacetylase 3 in Friedreich's ataxia gene silencing

Heterochromatin: silence is golden.

Repeat-induced epigenetic changes in intron 1 of the frataxin gene and its consequences in Friedreich ataxia

Suberoylanilide hydroxamic acid (SAHA; vorinostat) suppresses translation of cyclin D1 in mantle cell lymphoma cells.

Remodeling chromatin and stress resistance in the central nervous system: histone deacetylase inhibitors as novel and broadly effective neuroprotective agents.

Histone deacetylase inhibitors: molecular mechanisms of action.

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