Targeting ATM ameliorates mutant Huntingtin toxicity in cell and animal models of Huntington's disease.
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Targeting New Candidate Genes by Small Molecules Approaching Neurodegenerative DiseasesUtility of Induced Pluripotent Stem Cells for the Study and Treatment of Genetic Diseases: Focus on Childhood Neurological DisordersIs Huntingtin Dispensable in the Adult Brain?Induced Pluripotent Stem Cells: Global Research Trends.Genomic Instability Associated with p53 Knockdown in the Generation of Huntington's Disease Human Induced Pluripotent Stem CellsEarly-onset sleep defects in Drosophila models of Huntington's disease reflect alterations of PKA/CREB signaling.Polycomb repressive complex 2 (PRC2) silences genes responsible for neurodegeneration.Oxidative Stress and Huntington's Disease: The Good, The Bad, and The Ugly.Pluripotent stem cells in disease modelling and drug discovery.A new era of disease modeling and drug discovery using induced pluripotent stem cells.Huntington Disease as a Neurodevelopmental Disorder and Early Signs of the Disease in Stem Cells.Modeling simple repeat expansion diseases with iPSC technology.Induced Pluripotent Stem Cells in Huntington's Disease Research: Progress and Opportunity.Chronic oxidative damage together with genome repair deficiency in the neurons is a double whammy for neurodegeneration: Is damage response signaling a potential therapeutic target?Inhibiting sphingosine kinase 2 mitigates mutant Huntingtin-induced neurodegeneration in neuron models of Huntington disease.Generation of Cholinergic and Dopaminergic Interneurons from Human Pluripotent Stem Cells as a Relevant Tool for In Vitro Modeling of Neurological Disorders Pathology and Therapy.Huntingtin N17 domain is a reactive oxygen species sensor regulating huntingtin phosphorylation and localization.Optimization of trans-Splicing for Huntington's Disease RNA Therapy.Life and death rest on a bivalent chromatin state.Huntingtin is a scaffolding protein in the ATM oxidative DNA damage response complex.Huntington disease: Banking on ATM.Inhibition of PIP4Kγ ameliorates the pathological effects of mutant huntingtin protein.Integrated genomics and proteomics define huntingtin CAG length-dependent networks in mice.Striatal neurons directly converted from Huntington's disease patient fibroblasts recapitulate age-associated disease phenotypes.Polyglutamine-Expanded Huntingtin Exacerbates Age-Related Disruption of Nuclear Integrity and Nucleocytoplasmic Transport.DNA REPAIR. Drugging DNA repair.A unifying mechanism in neurodegeneration
P2860
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P2860
Targeting ATM ameliorates mutant Huntingtin toxicity in cell and animal models of Huntington's disease.
description
2014 nî lūn-bûn
@nan
2014年の論文
@ja
2014年論文
@yue
2014年論文
@zh-hant
2014年論文
@zh-hk
2014年論文
@zh-mo
2014年論文
@zh-tw
2014年论文
@wuu
2014年论文
@zh
2014年论文
@zh-cn
name
Targeting ATM ameliorates muta ...... odels of Huntington's disease.
@en
type
label
Targeting ATM ameliorates muta ...... odels of Huntington's disease.
@en
prefLabel
Targeting ATM ameliorates muta ...... odels of Huntington's disease.
@en
P2093
P2860
P50
P1476
Targeting ATM ameliorates muta ...... odels of Huntington's disease.
@en
P2093
Alex Osmand
Clive N Svendsen
David F Fischer
Erin Greiner
Ethan Signer
Ignacio Munoz-Sanjuan
Ismael Al-Ramahi
Jingbo Xiao
Juan Botas
Juan J Marugan
P2860
P304
P356
10.1126/SCITRANSLMED.3010523
P407
P577
2014-12-01T00:00:00Z