Ube3a mRNA and protein expression are not decreased in Mecp2R168X mutant mice
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Emerging pharmacotherapies for neurodevelopmental disordersFemale Mecp2(+/-) mice display robust behavioral deficits on two different genetic backgrounds providing a framework for pre-clinical studies.Beyond Widespread Mecp2 Deletions to Model Rett Syndrome: Conditional Spatio-Temporal Knockout, Single-Point Mutations and Transgenic Rescue MicePreclinical 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.Abnormalities of cell packing density and dendritic complexity in the MeCP2 A140V mouse model of Rett syndrome/X-linked mental retardationMeCP2 functions largely cell-autonomously, but also non-cell-autonomously, in neuronal maturation and dendritic arborization of cortical pyramidal neurons.Effect of Sarizotan, a 5-HT1a and D2-like receptor agonist, on respiration in three mouse models of Rett syndromeRespiratory phenotypes are distinctly affected in mice with common Rett syndrome mutations MeCP2 T158A and R168X.Temporal and regional alterations in NMDA receptor expression in Mecp2-null mice.Experimental models of Rett syndrome based on Mecp2 dysfunction.Characterization of the MeCP2R168X knockin mouse model for Rett syndrome.Complexities of Rett syndrome and MeCP2Rett syndrome like phenotypes in the R255X Mecp2 mutant mouse are rescued by MECP2 transgeneImpaired CO2 sensitivity of astrocytes in a mouse model of Rett syndrome.The relationship of Rett syndrome and MECP2 disorders to autism.Rescue of behavioral and EEG deficits in male and female Mecp2-deficient mice by delayed Mecp2 gene reactivation.Genes related to mitochondrial functions, protein degradation, and chromatin folding are differentially expressed in lymphomonocytes of Rett syndrome patientsMeCP2-Related Diseases and Animal Models.Behavioral profiles of mouse models for autism spectrum disorders.Rett syndrome and MeCP2.[Epigenetic regulation in neuronal differentiation and brain function].Defects in brainstem neurons associated with breathing and motor function in the Mecp2R168X/Y mouse model of Rett syndrome.MeCP2: only 100% will do.MeCP2 R168X male and female mutant mice exhibit Rett-like behavioral deficits.Rett syndrome: a neurological disorder with metabolic components.Gene therapy for Rett syndrome: prospects and challengesRett Syndrome: Coming to Terms with Treatment
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Ube3a mRNA and protein expression are not decreased in Mecp2R168X mutant mice
description
article científic
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article scientifique
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articolo scientifico
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artigo científico
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bilimsel makale
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scientific article published on 24 August 2007
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vedecký článok
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vetenskaplig artikel
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videnskabelig artikel
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vědecký článek
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name
Ube3a mRNA and protein expression are not decreased in Mecp2R168X mutant mice
@en
Ube3a mRNA and protein expression are not decreased in Mecp2R168X mutant mice.
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type
label
Ube3a mRNA and protein expression are not decreased in Mecp2R168X mutant mice
@en
Ube3a mRNA and protein expression are not decreased in Mecp2R168X mutant mice.
@nl
prefLabel
Ube3a mRNA and protein expression are not decreased in Mecp2R168X mutant mice
@en
Ube3a mRNA and protein expression are not decreased in Mecp2R168X mutant mice.
@nl
P2093
P2860
P1433
P1476
Ube3a mRNA and protein expression are not decreased in Mecp2R168X mutant mice
@en
P2093
Alo C Basu
Amy Lawson-Yuen
Daniel Liu
Guochuan E Tsai
Jiamin Feng
Jonathan Picker
Joseph T Coyle
Zhichun I Jiang
P2860
P356
10.1016/J.BRAINRES.2007.08.039
P407
P577
2007-08-24T00:00:00Z