Truncation of Ube3a-ATS unsilences paternal Ube3a and ameliorates behavioral defects in the Angelman syndrome mouse model - Test2 - elhamkhani - TriplyDB

Truncation of Ube3a-ATS unsilences paternal Ube3a and ameliorates behavioral defects in the Angelman syndrome mouse model

Truncation of Ube3a-ATS unsilences paternal Ube3a and ameliorates behavioral defects in the Angelman syndrome mouse model

http://www.wikidata.org/entity/Q35079892

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Prader-Willi, Angelman, and 15q11-q13 Duplication Syndromes The prospect of molecular therapy for Angelman syndrome and other monogenic neurologic disorders LncRNAs: emerging players in gene regulation and disease pathogenesis Association of new deletion/duplication region at chromosome 1p21 with intellectual disability, severe speech deficit and autism spectrum disorder-like behavior: an all-in approach to solving the DPYD enigma Seizure-like activity in a juvenile Angelman syndrome mouse model is attenuated by reducing Arc expression.Angelman syndrome imprinting center encodes a transcriptional promoter.Genomic imprinting does not reduce the dosage of UBE3A in neurons.E3 Ubiquitin Ligases Neurobiological Mechanisms: Development to Degeneration Differential regulation of non-protein coding RNAs from Prader-Willi Syndrome locus.Ube3a imprinting impairs circadian robustness in Angelman syndrome models Towards a therapy for Angelman syndrome by targeting a long non-coding RNA.Toward a Broader View of Ube3a in a Mouse Model of Angelman Syndrome: Expression in Brain, Spinal Cord, Sciatic Nerve and Glial Cells.Ube3a reinstatement identifies distinct developmental windows in a murine Angelman syndrome model.Angelman Syndrome.Of mothers and myelin: Aberrant myelination phenotypes in mouse model of Angelman syndrome are dependent on maternal and dietary influences Topoisomerase 1 Regulates Gene Expression in Neurons through Cleavage Complex-Dependent and -Independent Mechanisms.Variation in Dube3a expression affects neurotransmission at the Drosophila neuromuscular junction.Neurodevelopmental Underpinnings of Angelman Syndrome.Protein Delivery of an Artificial Transcription Factor Restores Widespread Ube3a Expression in an Angelman Syndrome Mouse Brain Potential therapeutic approaches for Angelman syndrome.Angelman syndrome-derived neurons display late onset of paternal UBE3A silencing.Mutation Update for UBE3A variants in Angelman syndrome.A role for chromatin topology in imprinted domain regulation.Strain-dependence of the Angelman Syndrome phenotypes in Ube3a maternal deficiency mice.Gene-targeting pharmaceuticals for single-gene disorders.A human haploid gene trap collection to study lncRNAs with unusual RNA biology Angelman syndrome: Current and emerging therapies in 2016.Epigenetic Mistakes in Neurodevelopmental Disorders.Box C/D small nucleolar RNA genes and the Prader-Willi syndrome: a complex interplay.Long noncoding RNA and its contribution to autism spectrum disorders.SNX15 Regulates Cell Surface Recycling of APP and Aβ Generation.Comparison of two types of non-adherent plate for neuronal differentiation of mouse embryonic stem cells.Neuronal overexpression of Ube3a isoform 2 causes behavioral impairments and neuroanatomical pathology relevant to 15q11.2-q13.3 duplication syndrome.Pharmacological therapies for Angelman syndrome.Forging our understanding of lncRNAs in the brain.Enhanced Nociception in Angelman Syndrome Model Mice.Antisense Activity across the Nesp Promoter is Required for Nespas-Mediated Silencing in the Imprinted Gnas Cluster.Epigenetics and Human Disease.A behavioral test battery for mouse models of Angelman syndrome: a powerful tool for testing drugs and novel mutants

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Truncation of Ube3a-ATS unsilences paternal Ube3a and ameliorates behavioral defects in the Angelman syndrome mouse model

http://www.wikidata.org/entity/Q35079892

description

2013 nî lūn-bûn

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2013 թուականի Դեկտեմբերին հրատարակուած գիտական յօդուած

@hyw

2013 թվականի դեկտեմբերին հրատարակված գիտական հոդված

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2013年の論文

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2013年論文

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2013年論文

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2013年論文

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2013年論文

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2013年論文

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2013年论文

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Truncation of Ube3a-ATS unsile ...... Angelman syndrome mouse model

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Truncation of Ube3a-ATS unsile ...... Angelman syndrome mouse model

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Truncation of Ube3a-ATS unsile ...... Angelman syndrome mouse model

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Truncation of Ube3a-ATS unsile ...... Angelman syndrome mouse model

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Truncation of Ube3a-ATS unsile ...... Angelman syndrome mouse model

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Truncation of Ube3a-ATS unsile ...... Angelman syndrome mouse model

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Truncation of Ube3a-ATS unsile ...... Angelman syndrome mouse model

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P2093

Arthur L Beaudet

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Linyan Meng

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Mauro Costa-Mattioli

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Ping Jun Zhu

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

Richard Erwin Person

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Wei Huang

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

P2860

Elongation of the Kcnq1ot1 transcript is required for genomic imprinting of neighboring genes

Topoisomerase inhibitors unsilence the dormant allele of Ube3a in neurons

Angelman syndrome: insights into genomic imprinting and neurodevelopmental phenotypes

Suppression of PKR promotes network excitability and enhanced cognition by interferon-γ-mediated disinhibition

Collision events between RNA polymerases in convergent transcription studied by atomic force microscopy

Altered ultrasonic vocalization and impaired learning and memory in Angelman syndrome mouse model with a large maternal deletion from Ube3a to Gabrb3.

Nascent transcript sequencing visualizes transcription at nucleotide resolution.

The human necdin gene, NDN, is maternally imprinted and located in the Prader-Willi syndrome chromosomal region

A mixed epigenetic/genetic model for oligogenic inheritance of autism with a limited role for UBE3A

The spectrum of mutations in UBE3A causing Angelman syndrome

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3873245

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