Elevated methyl-CpG-binding protein 2 expression is acquired during postnatal human brain development and is correlated with alternative polyadenylation. - Wikidata - awgldk - TriplyDB

Elevated methyl-CpG-binding protein 2 expression is acquired during postnatal human brain development and is correlated with alternative polyadenylation.

Elevated methyl-CpG-binding protein 2 expression is acquired during postnatal human brain development and is correlated with alternative polyadenylation.

http://www.wikidata.org/entity/Q31126823

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Epigenetic overlap in autism-spectrum neurodevelopmental disorders: MECP2 deficiency causes reduced expression of UBE3A and GABRB3.Reciprocal co-regulation of EGR2 and MECP2 is disrupted in Rett syndrome and autism The odyssey of MeCP2 and parental imprinting Inhibitors of differentiation (ID1, ID2, ID3 and ID4) genes are neuronal targets of MeCP2 that are elevated in Rett syndrome Developmental Dynamics of Rett Syndrome BDNF deregulation in Rett syndrome Rett syndrome: a prototypical neurodevelopmental disorder MeCP2-dependent repression of an imprinted miR-184 released by depolarization A critical and cell-autonomous role for MeCP2 in synaptic scaling up Reduced MeCP2 expression is frequent in autism frontal cortex and correlates with aberrant MECP2 promoter methylation High levels of MeCP2 depress MHC class I expression in neuronal cells.The Crucial Role of DNA Methylation and MeCP2 in Neuronal Function The role of MeCP2 in brain development and neurodevelopmental disorders Ocular MECP2 protein expression in patients with and without Rett syndrome.MeCP2 mutation results in compartment-specific reductions in dendritic branching and spine density in layer 5 motor cortical neurons of YFP-H mice.Cell-autonomous alterations in dendritic arbor morphology and connectivity induced by overexpression of MeCP2 in Xenopus central neurons in vivo MeCP2 dependent heterochromatin reorganization during neural differentiation of a novel Mecp2-deficient embryonic stem cell reporter line.Setdb1-mediated histone H3K9 hypermethylation in neurons worsens the neurological phenotype of Mecp2-deficient mice.Astrocyte-specific regulation of hMeCP2 expression in Drosophila.Gestational hypoxia and epigenetic programming of brain development disorders.MeCP2 is required for global heterochromatic and nucleolar changes during activity-dependent neuronal maturation.Neuronal MeCP2 is expressed at near histone-octamer levels and globally alters the chromatin state.Rett syndrome: the complex nature of a monogenic disease.Genotype-specific effects of Mecp2 loss-of-function on morphology of Layer V pyramidal neurons in heterozygous female Rett syndrome model mice.CAGE-defined promoter regions of the genes implicated in Rett Syndrome.Dynamic changes in Histone H3 lysine 9 acetylation localization patterns during neuronal maturation require MeCP2.Synaptic dysfunction in neurodevelopmental disorders associated with autism and intellectual disabilities.Linking epigenetics to human disease and Rett syndrome: the emerging novel and challenging concepts in MeCP2 research.ALS mutations in TLS/FUS disrupt target gene expression.NUDT21-spanning CNVs lead to neuropsychiatric disease and altered MeCP2 abundance via alternative polyadenylation Phosphorylation of distinct sites in MeCP2 modifies cofactor associations and the dynamics of transcriptional regulation Regulatory functions and pathological relevance of the MECP2 3'UTR in the central nervous system.Generation of neuronal variability and complexity.Human-specific regulation of MeCP2 levels in fetal brains by microRNA miR-483-5p.MECP2 genomic structure and function: insights from ENCODE NMDA receptor regulation prevents regression of visual cortical function in the absence of Mecp2.Exposure to caregiver maltreatment alters expression levels of epigenetic regulators in the medial prefrontal cortex.Brain-expressed 3'UTR extensions strengthen miRNA cross-talk between ion channel/transporter encoding mRNAs.MeCP2-Related Diseases and Animal Models.Mediators and dynamics of DNA methylation.

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P2860

Elevated methyl-CpG-binding protein 2 expression is acquired during postnatal human brain development and is correlated with alternative polyadenylation.

http://www.wikidata.org/entity/Q31126823

description

2002 nî lūn-bûn

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2002 թուականի Դեկտեմբերին հրատարակուած գիտական յօդուած

@hyw

2002 թվականի դեկտեմբերին հրատարակված գիտական հոդված

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2002年の論文

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2002年論文

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2002年論文

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2002年論文

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2002年論文

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2002年論文

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2002年论文

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name

Elevated methyl-CpG-binding pr ...... h alternative polyadenylation.

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type

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Elevated methyl-CpG-binding pr ...... h alternative polyadenylation.

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Elevated methyl-CpG-binding pr ...... h alternative polyadenylation.

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Elevated methyl-CpG-binding pr ...... h alternative polyadenylation.

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P1433

Journal of Molecular Medicine

P1476

Elevated methyl-CpG-binding pr ...... th alternative polyadenylation

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P2093

Damina Balmer

http://www.w3.org/2001/XMLSchema#string

Jared Goldstine

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Y Manjula Rao

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P2860

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

Regulation of gene expression for translation initiation factor eIF-2 alpha: importance of the 3' untranslated region

Characterization of MeCP2, a vertebrate DNA binding protein with affinity for methylated DNA

Comparative sequence analysis of the MECP2-locus in human and mouse reveals new transcribed regions

Purification, sequence, and cellular localization of a novel chromosomal protein that binds to methylated DNA

A mouse Mecp2-null mutation causes neurological symptoms that mimic Rett syndrome

Insight into Rett syndrome: MeCP2 levels display tissue- and cell-specific differences and correlate with neuronal maturation

MeCP2 is a transcriptional repressor with abundant binding sites in genomic chromatin

Deficiency of methyl-CpG binding protein-2 in CNS neurons results in a Rett-like phenotype in mice

Mice with truncated MeCP2 recapitulate many Rett syndrome features and display hyperacetylation of histone H3

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s00109-002-0396-5

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1

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