about
Dynamics, stability and iron-binding activity of frataxin clinical mutantsTherapeutic developments in Friedreich ataxiaMeasuring the rate of progression in Friedreich ataxia: implications for clinical trial design.Friedreich's ataxia: iron chelators that target the mitochondrion as a therapeutic strategy?An AAV9 coding for frataxin clearly improved the symptoms and prolonged the life of Friedreich ataxia mouse modelsIdebenone and reduced cardiac hypertrophy in Friedreich's ataxiaFrataxin, iron-sulfur clusters, heme, ROS, and aging.Cerebrospinal Fluid Biomarkers in Spinocerebellar Ataxia: A Pilot Study.Frataxin levels in peripheral tissue in Friedreich ataxia.Hydrogen peroxide scavenging rescues frataxin deficiency in a Drosophila model of Friedreich's ataxia.PCTH: a novel orally active chelator for the treatment of iron overload disease.Friedreich ataxia clinical outcome measures: natural history evaluation in 410 participantsTranslocation and deletion breakpoints in cancer genomes are associated with potential non-B DNA-forming sequencesThe mitochondrial connection in auditory neuropathy.Management and therapy for cardiomyopathy in Friedreich's ataxia.Therapeutic approaches for the treatment of Friedreich's ataxia.Pharmacological therapeutics in Friedreich ataxia: the present state.A Potential New Therapeutic Approach for Friedreich Ataxia: Induction of Frataxin Expression With TALE Proteins.Replication stalling at Friedreich's ataxia (GAA)n repeats in vivo.Diagnosis and Genetic Counseling for Friedreich's Ataxia: A time for consideration of TP-PCR in an Indian Setup.Conformational stability of human frataxin and effect of Friedreich's ataxia-related mutations on protein folding.Iron and Sex Cross Paths in the Heart.Glutathione in blood of patients with Friedreich's ataxia.Friedreich's ataxia associated with mitochondrial myopathy: clinicopathologic report.Analysis of the visual system in Friedreich ataxia.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.Early cerebellar deficits in mitochondrial biogenesis and respiratory chain complexes in the KIKO mouse model of Friedreich ataxia.PEP-1-frataxin significantly increases cell proliferation and neuroblast differentiation by reducing lipid peroxidation in the mouse dentate gyrus.
P2860
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P2860
description
1999 nî lūn-bûn
@nan
1999 թուականի Հոկտեմբերին հրատարակուած գիտական յօդուած
@hyw
1999 թվականի հոտեմբերին հրատարակված գիտական հոդված
@hy
1999年の論文
@ja
1999年論文
@yue
1999年論文
@zh-hant
1999年論文
@zh-hk
1999年論文
@zh-mo
1999年論文
@zh-tw
1999年论文
@wuu
name
Molecular pathogenesis of Friedreich ataxia.
@ast
Molecular pathogenesis of Friedreich ataxia.
@en
type
label
Molecular pathogenesis of Friedreich ataxia.
@ast
Molecular pathogenesis of Friedreich ataxia.
@en
prefLabel
Molecular pathogenesis of Friedreich ataxia.
@ast
Molecular pathogenesis of Friedreich ataxia.
@en
P1433
P1476
Molecular pathogenesis of Friedreich ataxia.
@en
P2093
Pandolfo M
P304
P356
10.1001/ARCHNEUR.56.10.1201
P577
1999-10-01T00:00:00Z