MeCP2 is critical within HoxB1-derived tissues of mice for normal lifespan - Wikidata - thesis-toulmin - TriplyDB

MeCP2 is critical within HoxB1-derived tissues of mice for normal lifespan

MeCP2 is critical within HoxB1-derived tissues of mice for normal lifespan

http://www.wikidata.org/entity/Q35219982

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Daily rhythmic behaviors and thermoregulatory patterns are disrupted in adult female MeCP2-deficient mice Disturbance of cardiac gene expression and cardiomyocyte structure predisposes Mecp2-null mice to arrhythmias Loss of MeCP2 in the rat models regression, impaired sociability and transcriptional deficits of Rett syndrome.Loss of MeCP2 in Parvalbumin-and Somatostatin-Expressing Neurons in Mice Leads to Distinct Rett Syndrome-like Phenotypes Manipulations of MeCP2 in glutamatergic neurons highlight their contributions to Rett and other neurological disorders Cellular origins of auditory event-related potential deficits in Rett syndrome Insulinotropic treatments exacerbate metabolic syndrome in mice lacking MeCP2 function.Female Mecp2(+/-) mice display robust behavioral deficits on two different genetic backgrounds providing a framework for pre-clinical studies.Brain activity mapping in Mecp2 mutant mice reveals functional deficits in forebrain circuits, including key nodes in the default mode network, that are reversed with ketamine treatment.Preclinical research in Rett syndrome: setting the foundation for translational success.Twenty-four hour quantitative-EEG and in-vivo glutamate biosensor detects activity and circadian rhythm dependent biomarkers of pathogenesis in Mecp2 null mice.Redox imbalance and morphological changes in skin fibroblasts in typical 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.Functional recovery with recombinant human IGF1 treatment in a mouse model of Rett Syndrome.Treatment of cardiac arrhythmias in a mouse model of Rett syndrome with Na+-channel-blocking antiepileptic drugs.Rett syndrome like phenotypes in the R255X Mecp2 mutant mouse are rescued by MECP2 transgene Loss of MeCP2 Causes Urological Dysfunction and Contributes to Death by Kidney Failure in Mouse Models of Rett Syndrome.The relationship of Rett syndrome and MECP2 disorders to autism.Reduction of aberrant NF-κB signalling ameliorates Rett syndrome phenotypes in Mecp2-null mice.A Role for Diminished GABA Transporter Activity in the Cortical Discharge Phenotype of MeCP2-Deficient Mice.Progressive Changes in a Distributed Neural Circuit Underlie Breathing Abnormalities in Mice Lacking MeCP2.A TrkB small molecule partial agonist rescues TrkB phosphorylation deficits and improves respiratory function in a mouse model of Rett syndrome Loss of MeCP2 function is associated with distinct gene expression changes in the striatum Breathing challenges in Rett syndrome: lessons learned from humans and animal models.Rescue of behavioral and EEG deficits in male and female Mecp2-deficient mice by delayed Mecp2 gene reactivation.Alterations in the carnitine cycle in a mouse model of Rett syndrome.Neurotrophic factors in development and regulation of respiratory control.Rett syndrome: a complex disorder with simple roots.Embryonic hindbrain patterning genes delineate distinct cardio-respiratory and metabolic homeostatic populations in the adult Body Temperature Measurements for Metabolic Phenotyping in Mice.Genetic and Pharmacological Reversibility of Phenotypes in Mouse Models of Autism Spectrum Disorder.Pathogenesis of Lethal Aspiration Pneumonia in Mecp2-null Mouse Model for Rett Syndrome Early motor phenotype detection in a female mouse model of Rett syndrome is improved by cross-fostering.Motor, Somatosensory, Viscerosensory and Metabolic Impairments in a Heterozygous Female Rat Model of Rett Syndrome.Stem Cell Technology for (Epi)genetic Brain Disorders.Methyl-CpG binding-protein 2 function in cholinergic neurons mediates cardiac arrhythmogenesis.Selective preservation of MeCP2 in catecholaminergic cells is sufficient to improve the behavioral phenotype of male and female Mecp2-deficient mice.Motor neuron degeneration correlates with respiratory dysfunction in SCA1.Epigenetics and Human Disease.

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MeCP2 is critical within HoxB1-derived tissues of mice for normal lifespan

http://www.wikidata.org/entity/Q35219982

description

2011 nî lūn-bûn

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2011 թուականի Յուլիսին հրատարակուած գիտական յօդուած

@hyw

2011 թվականի հուլիսին հրատարակված գիտական հոդված

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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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name

MeCP2 is critical within HoxB1-derived tissues of mice for normal lifespan

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MeCP2 is critical within HoxB1-derived tissues of mice for normal lifespan

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type

label

MeCP2 is critical within HoxB1-derived tissues of mice for normal lifespan

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MeCP2 is critical within HoxB1-derived tissues of mice for normal lifespan

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prefLabel

MeCP2 is critical within HoxB1-derived tissues of mice for normal lifespan

@ast

MeCP2 is critical within HoxB1-derived tissues of mice for normal lifespan

@en

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P356

JNEUROSCI.0057-11.2011

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Journal of Neuroscience

P1476

MeCP2 is critical within HoxB1-derived tissues of mice for normal lifespan

@en

P2093

E Melissa Arvide

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

Jong Yoo

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Teng-Wei Huang

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P2860

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

Rett syndrome: revised diagnostic criteria and nomenclature

Loss of MeCP2 in aminergic neurons causes cell-autonomous defects in neurotransmitter synthesis and specific behavioral abnormalities

A developmental switch in the response of DRG neurons to ETS transcription factor signaling

Generalized lacZ expression with the ROSA26 Cre reporter strain

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

Mecp2 deficiency disrupts norepinephrine and respiratory systems in mice

A partial loss of function allele of methyl-CpG-binding protein 2 predicts a human neurodevelopmental syndrome

Dysfunction in GABA signalling mediates autism-like stereotypies and Rett syndrome phenotypes

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

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10359-10370

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scholarly article

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10.1523/JNEUROSCI.0057-11.2011

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28

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31

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Christopher S. Ward

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Jeffrey L. Neul

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51489371

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21753013

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3175623

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