Rett syndrome mutation MeCP2 T158A disrupts DNA binding, protein stability and ERP responses - Test2 - elhamkhani - TriplyDB

Rett syndrome mutation MeCP2 T158A disrupts DNA binding, protein stability and ERP responses

Rett syndrome mutation MeCP2 T158A disrupts DNA binding, protein stability and ERP responses

http://www.wikidata.org/entity/Q30465294

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BDNF deregulation in Rett syndrome A review of Rett syndrome (RTT) with induced pluripotent stem cells Rett syndrome mutations abolish the interaction of MeCP2 with the NCoR/SMRT co-repressor FoxO6 regulates memory consolidation and synaptic function MeCP2 deficiency results in robust Rett-like behavioural and motor deficits in male and female rats Sensory processing in autism spectrum disorders and Fragile X syndrome-From the clinic to animal models.Loss of MeCP2 in the rat models regression, impaired sociability and transcriptional deficits of Rett syndrome.Degraded neural and behavioral processing of speech sounds in a rat model of Rett syndrome.Automatic cortical representation of auditory pitch changes in Rett syndrome.Characterization of Rett Syndrome-like phenotypes in Mecp2-knockout rats Induced gamma oscillations differentiate familiar and novel voices in children with MECP2 duplication and Rett syndromes.Cellular origins of auditory event-related potential deficits in Rett syndrome Beyond Widespread Mecp2 Deletions to Model Rett Syndrome: Conditional Spatio-Temporal Knockout, Single-Point Mutations and Transgenic Rescue Mice Preclinical research in Rett syndrome: setting the foundation for translational success.Mice with an isoform-ablating Mecp2 exon 1 mutation recapitulate the neurologic deficits of Rett syndrome.Structure of the MeCP2-TBLR1 complex reveals a molecular basis for Rett syndrome and related disorders.Development of a Novel AAV Gene Therapy Cassette with Improved Safety Features and Efficacy in a Mouse Model of Rett Syndrome Improved MECP2 Gene Therapy Extends the Survival of MeCP2-Null Mice without Apparent Toxicity after Intracisternal Delivery.The Crucial Role of DNA Methylation and MeCP2 in Neuronal Function Oxidative brain damage in Mecp2-mutant murine models of Rett syndrome The neural circuit basis of Rett syndrome Respiratory phenotypes are distinctly affected in mice with common Rett syndrome mutations MeCP2 T158A and R168X.Overview of mouse models of autism spectrum disorders Gestational hypoxia and epigenetic programming of brain development disorders.Characterization of the MeCP2R168X knockin mouse model for Rett syndrome.Rett syndrome like phenotypes in the R255X Mecp2 mutant mouse are rescued by MECP2 transgene Circadian cycle-dependent MeCP2 and brain chromatin changes Genotype-specific effects of Mecp2 loss-of-function on morphology of Layer V pyramidal neurons in heterozygous female Rett syndrome model mice.The methyl-CpG-binding domain (MBD) is crucial for MeCP2's dysfunction-induced defects in adult newborn neurons Physics-Based Potentials for Coarse-Grained Modeling of Protein-DNA Interactions Rett syndrome: genes, synapses, circuits, and therapeutics MeCP2 Related Studies Benefit from the Use of CD1 as Genetic Background.MicroRNAs downregulated in neuropathic pain regulate MeCP2 and BDNF related to pain sensitivity.Characterization of spatio-temporal epidural event-related potentials for mouse models of psychiatric disorders.Phosphorylation of MeCP2 at Ser421 contributes to chronic antidepressant action.The relationship of Rett syndrome and MECP2 disorders to autism.Loss of CDKL5 disrupts kinome profile and event-related potentials leading to autistic-like phenotypes in mice.The molecular basis of variable phenotypic severity among common missense mutations causing Rett syndrome MeCP2 SUMOylation rescues Mecp2-mutant-induced behavioural deficits in a mouse model of Rett syndrome.Epigenetic mechanisms in neurological disease

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Rett syndrome mutation MeCP2 T158A disrupts DNA binding, protein stability and ERP responses

http://www.wikidata.org/entity/Q30465294

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2011 nî lūn-bûn

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2011 թուականի Նոյեմբերին հրատարակուած գիտական յօդուած

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2011年の論文

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2011年論文

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2011年論文

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2011年论文

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Rett syndrome mutation MeCP2 T ...... in stability and ERP responses

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Rett syndrome mutation MeCP2 T ...... in stability and ERP responses

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Rett syndrome mutation MeCP2 T ...... in stability and ERP responses

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Rett syndrome mutation MeCP2 T ...... in stability and ERP responses

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Rett syndrome mutation MeCP2 T ...... in stability and ERP responses

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Rett syndrome mutation MeCP2 T ...... in stability and ERP responses

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Nature Neuroscience

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Rett syndrome mutation MeCP2 T ...... in stability and ERP responses

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Amy Mercado-Berton

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Arith-Ruth S Reyes

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Caroline Ong

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Gregory C Carlson

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I-Ting Judy Wang

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Julie A Blendy

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Le Zhang

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Linda Hu

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Maria Amorim

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Megan Allen

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P2860

Rett syndrome is caused by mutations in X-linked MECP2, encoding methyl-CpG-binding protein 2

Transcriptional repression by the methyl-CpG-binding protein MeCP2 involves a histone deacetylase complex

Reduced cortical activity due to a shift in the balance between excitation and inhibition in a mouse model of Rett syndrome

MeCP2, a key contributor to neurological disease, activates and represses transcription

MeCP2 binding to DNA depends upon hydration at methyl-CpG

Oscillatory gamma activity in humans and its role in object representation

Molecular genetics of Rett syndrome: when DNA methylation goes unrecognized

Phenotypic manifestations of MECP2 mutations in classical and atypical Rett syndrome

The story of Rett syndrome: from clinic to neurobiology

Neuronal oscillations in cortical networks

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274-283

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10.1038/NN.2997

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2

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15

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Steven J. Siegel

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2011-11-27T00:00:00Z

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51836749

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22119903

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3267879

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