Impairment of developmental stem cell-mediated striatal neurogenesis and pluripotency genes in a knock-in model of Huntington's disease
about
Mind the gap: models in multiple species needed for therapeutic development in Huntington's diseaseModeling Huntington's disease with induced pluripotent stem cellsEpigenetics and therapeutic targets mediating neuroprotectionA broad phenotypic screen identifies novel phenotypes driven by a single mutant allele in Huntington's disease CAG knock-in mice.Huntingtin Is Required for Neural But Not Cardiac/Pancreatic Progenitor Differentiation of Mouse Embryonic Stem Cells In vitro.Multiple phenotypes in Huntington disease mouse neural stem cells.Anaesthetics-induced neurotoxicity in developing brain: an update on preclinical evidence.Corepressor for element-1-silencing transcription factor preferentially mediates gene networks underlying neural stem cell fate decisions.Cerebral cortex structure in prodromal Huntington disease.Smaller intracranial volume in prodromal Huntington's disease: evidence for abnormal neurodevelopment.REST and CoREST are transcriptional and epigenetic regulators of seminal neural fate decisions.Selective roles of normal and mutant huntingtin in neural induction and early neurogenesisFunctions of huntingtin in germ layer specification and organogenesis.Striatal neurons expressing full-length mutant huntingtin exhibit decreased N-cadherin and altered neuritogenesis.Phenotyping dividing cells in mouse models of neurodegenerative basal ganglia diseases.Correlation of CAG repeat length between the maternal and paternal allele of the Huntingtin gene: evidence for assortative mating.HD iPSC-derived neural progenitors accumulate in culture and are susceptible to BDNF withdrawal due to glutamate toxicity.Homeobox genes in obsessive-compulsive disorder.Huntington disease iPSCs show early molecular changes in intracellular signaling, the expression of oxidative stress proteins and the p53 pathwayMeasures of growth in children at risk for Huntington diseaseHuntington's Disease as Neurodevelopmental Disorder: Altered Chromatin Regulation, Coding, and Non-Coding RNA Transcription.Extensive changes in DNA methylation are associated with expression of mutant huntingtin.Selective expression of mutant huntingtin during development recapitulates characteristic features of Huntington's diseaseMolecular mechanisms and potential therapeutical targets in Huntington's disease.The multiplicity of action of cannabinoids: implications for treating neurodegeneration.Huntington's disease: can mice lead the way to treatment?Utilization of neural stem cell-derived models to study anesthesia-related toxicity and preventative approaches.The influence of cannabinoids on generic traits of neurodegeneration.Huntington Disease as a Neurodevelopmental Disorder and Early Signs of the Disease in Stem Cells.Genomic Analysis Reveals Disruption of Striatal Neuronal Development and Therapeutic Targets in Human Huntington's Disease Neural Stem Cells.Long Term Aggresome Accumulation Leads to DNA Damage, p53-dependent Cell Cycle Arrest, and Steric Interference in Mitosis.Developmental alterations in Huntington's disease neural cells and pharmacological rescue in cells and mice.Similar Progression of Morphological and Metabolic Phenotype in R6/2 Mice with Different CAG Repeats Revealed by In Vivo Magnetic Resonance Imaging and Spectroscopy.Cholinergic interneurons in the Q140 knockin mouse model of Huntington's disease: Reductions in dendritic branching and thalamostriatal input.The Generation of Mouse and Human Huntington Disease iPS Cells Suitable for In vitro Studies on Huntingtin FunctionHedgehog controls neural stem cells through p53-independent regulation of Nanog.Induced pluripotent stem cells from patients with Huntington's disease show CAG-repeat-expansion-associated phenotypes.Adult neural progenitor cells from Huntington's disease mouse brain exhibit increased proliferation and migration due to enhanced calcium and ROS signals.Postnatal and adult consequences of loss of huntingtin during development: Implications for Huntington's disease.Early postnatal behavioral, cellular, and molecular changes in models of Huntington disease are reversible by HDAC inhibition
P2860
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P2860
Impairment of developmental stem cell-mediated striatal neurogenesis and pluripotency genes in a knock-in model of Huntington's disease
description
2009 nî lūn-bûn
@nan
2009 թուականի Դեկտեմբերին հրատարակուած գիտական յօդուած
@hyw
2009 թվականի դեկտեմբերին հրատարակված գիտական հոդված
@hy
2009年の論文
@ja
2009年論文
@yue
2009年論文
@zh-hant
2009年論文
@zh-hk
2009年論文
@zh-mo
2009年論文
@zh-tw
2009年论文
@wuu
name
Impairment of developmental st ...... model of Huntington's disease
@ast
Impairment of developmental st ...... model of Huntington's disease
@en
Impairment of developmental st ...... model of Huntington's disease.
@nl
type
label
Impairment of developmental st ...... model of Huntington's disease
@ast
Impairment of developmental st ...... model of Huntington's disease
@en
Impairment of developmental st ...... model of Huntington's disease.
@nl
prefLabel
Impairment of developmental st ...... model of Huntington's disease
@ast
Impairment of developmental st ...... model of Huntington's disease
@en
Impairment of developmental st ...... model of Huntington's disease.
@nl
P2093
P2860
P356
P1476
Impairment of developmental st ...... model of Huntington's disease
@en
P2093
Jessica L Feig
Lucien C Alexandre
Mark F Mehler
Sara Gonzalez
Solen Gokhan
P2860
P304
21900-21905
P356
10.1073/PNAS.0912171106
P407
P577
2009-12-02T00:00:00Z