A gene expression phenotype in lymphocytes from Friedreich ataxia patients.
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Cardiomyopathy in Friedreich ataxia: clinical findings and researchAn epigenetic signature in peripheral blood associated with the haplotype on 17q21.31, a risk factor for neurodegenerative tauopathy.Mutation of senataxin alters disease-specific transcriptional networks in patients with ataxia with oculomotor apraxia type 2Novel frataxin isoforms may contribute to the pathological mechanism of Friedreich ataxiaQuantitative proteomic analysis identifies targets and pathways of a 2-aminobenzamide HDAC inhibitor in Friedreich's ataxia patient iPSC-derived neural stem cells.Epigenetic therapy for Friedreich ataxiaTranscriptome Profiling of Peripheral Blood in 22q11.2 Deletion Syndrome Reveals Functional Pathways Related to Psychosis and Autism Spectrum DisorderIdentification of telomere dysfunction in Friedreich ataxiaDNA methylation, insulin resistance and second-generation antipsychotics in bipolar disorder.Genetic ablation of homeodomain-interacting protein kinase 2 selectively induces apoptosis of cerebellar Purkinje cells during adulthood and generates an ataxic-like phenotype.Friedreich ataxia: new pathways.Degenerative Ataxias: challenges in clinical research.A review of Friedreich ataxia clinical trial results.Frataxin silencing inactivates mitochondrial Complex I in NSC34 motoneuronal cells and alters glutathione homeostasisTranslating HDAC inhibitors in Friedreich's ataxia.Excision of Expanded GAA Repeats Alleviates the Molecular Phenotype of Friedreich's Ataxia.Friedreich ataxia-induced pluripotent stem cell-derived neurons show a cellular phenotype that is corrected by a benzamide HDAC inhibitor.Novel candidate blood-based transcriptional biomarkers of Machado-Joseph disease.Comprehensive analysis of gene expression patterns in Friedreich's ataxia fibroblasts by RNA sequencing reveals altered levels of protein synthesis factors and solute carriers.Early cerebellar deficits in mitochondrial biogenesis and respiratory chain complexes in the KIKO mouse model of Friedreich ataxia.Inducible and reversible phenotypes in a novel mouse model of Friedreich's Ataxia.Synthetic transcription elongation factors license transcription across repressive chromatin.Long-term treatment with thiamine as possible medical therapy for Friedreich ataxia.Gene Expression Profile in Peripheral Blood Cells of Friedreich Ataxia Patients.Peripheral blood gene expression reveals an inflammatory transcriptomic signature in Friedreich's ataxia patients
P2860
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P2860
A gene expression phenotype in lymphocytes from Friedreich ataxia patients.
description
2011 nî lūn-bûn
@nan
2011年の論文
@ja
2011年論文
@yue
2011年論文
@zh-hant
2011年論文
@zh-hk
2011年論文
@zh-mo
2011年論文
@zh-tw
2011年论文
@wuu
2011年论文
@zh
2011年论文
@zh-cn
name
A gene expression phenotype in lymphocytes from Friedreich ataxia patients.
@en
type
label
A gene expression phenotype in lymphocytes from Friedreich ataxia patients.
@en
prefLabel
A gene expression phenotype in lymphocytes from Friedreich ataxia patients.
@en
P2093
P2860
P356
P1433
P1476
A gene expression phenotype in lymphocytes from Friedreich ataxia patients.
@en
P2093
Alessandro Filla
Daniel H Geschwind
David R Lynch
Francesco Saccá
Fuying Gao
Giovanni Coppola
Heather Plasterer
James R Rusche
Joel M Gottesfeld
Massimo Pandolfo
P2860
P304
P356
10.1002/ANA.22526
P577
2011-11-01T00:00:00Z