Gene expression profiling in frataxin deficient mice: microarray evidence for significant expression changes without detectable neurodegeneration
about
Modeling diseases of noncoding unstable repeat expansions using mutant pluripotent stem cells.Altered gene expression and DNA damage in peripheral blood cells from Friedreich's ataxia patients: cellular model of pathology.GAA repeat expansion mutation mouse models of Friedreich ataxia exhibit oxidative stress leading to progressive neuronal and cardiac pathology.Transcriptional analysis of the response of Neurospora crassa to phytosphingosine reveals links to mitochondrial function.Friedreich's ataxia induced pluripotent stem cells model intergenerational GAA⋅TTC triplet repeat instabilityDNA sequence-specific polyamides alleviate transcription inhibition associated with long GAA.TTC repeats in Friedreich's ataxia.A novel GAA-repeat-expansion-based mouse model of Friedreich's ataxiaMitochondrial Diseases Part II: Mouse models of OXPHOS deficiencies caused by defects in regulatory factors and other components required for mitochondrial function.Effects of carbonic anhydrase VIII deficiency on cerebellar gene expression profiles in the wdl mouse.A gene expression phenotype in lymphocytes from Friedreich ataxia patients.Advancements in the pathophysiology of Friedreich's Ataxia and new prospects for treatments.Friedreich ataxia: new pathways.Lateral-flow immunoassay for the frataxin protein in Friedreich's ataxia patients and carriers.Functional genomic analysis of frataxin deficiency reveals tissue-specific alterations and identifies the PPARgamma pathway as a therapeutic target in Friedreich's ataxia.Animal and cellular models of Friedreich ataxia.Diabetes in Friedreich ataxia.Frataxin silencing inactivates mitochondrial Complex I in NSC34 motoneuronal cells and alters glutathione homeostasisBacterial cell wall constituents induce hepcidin expression in macrophages through MyD88 signaling.Generation of induced pluripotent stem cell lines from Friedreich ataxia patients.Frataxin knockdown causes loss of cytoplasmic iron-sulfur cluster functions, redox alterations and induction of heme transcripts.Deletion of the GAA repeats from the human frataxin gene using the CRISPR-Cas9 system in YG8R-derived cells and mouse models of Friedreich ataxia.Neurobehavioral deficits in the KIKO mouse model of Friedreich's ataxia.Inducible and reversible phenotypes in a novel mouse model of Friedreich's Ataxia.
P2860
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P2860
Gene expression profiling in frataxin deficient mice: microarray evidence for significant expression changes without detectable neurodegeneration
description
2006 nî lūn-bûn
@nan
2006 թուականի Յունուարին հրատարակուած գիտական յօդուած
@hyw
2006 թվականի հունվարին հրատարակված գիտական հոդված
@hy
2006年の論文
@ja
2006年論文
@yue
2006年論文
@zh-hant
2006年論文
@zh-hk
2006年論文
@zh-mo
2006年論文
@zh-tw
2006年论文
@wuu
name
Gene expression profiling in f ...... t detectable neurodegeneration
@ast
Gene expression profiling in f ...... t detectable neurodegeneration
@en
type
label
Gene expression profiling in f ...... t detectable neurodegeneration
@ast
Gene expression profiling in f ...... t detectable neurodegeneration
@en
prefLabel
Gene expression profiling in f ...... t detectable neurodegeneration
@ast
Gene expression profiling in f ...... t detectable neurodegeneration
@en
P2093
P2860
P1476
Gene expression profiling in f ...... t detectable neurodegeneration
@en
P2093
Carlos J Miranda
Dmitri Tentler
Eric M Wexler
Giovanni Coppola
Manuela M Santos
Massimo Pandolfo
Sang-Hyun Choi
P2860
P304
P356
10.1016/J.NBD.2005.11.014
P577
2006-01-25T00:00:00Z