Gene expression signature of cerebellar hypoplasia in a mouse model of Down syndrome during postnatal development. - Wikidata - awgldk - TriplyDB

Gene expression signature of cerebellar hypoplasia in a mouse model of Down syndrome during postnatal development.

Gene expression signature of cerebellar hypoplasia in a mouse model of Down syndrome during postnatal development.

http://www.wikidata.org/entity/Q33424071

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DYRK1A, a Dosage-Sensitive Gene Involved in Neurodevelopmental Disorders, Is a Target for Drug Development in Down Syndrome Mouse models of Down syndrome as a tool to unravel the causes of mental disabilities PCP4 (PEP19) overexpression induces premature neuronal differentiation associated with Ca(2+) /calmodulin-dependent kinase II-δ activation in mouse models of Down syndrome.Expression in aneuploid Drosophila S2 cells.Comparable low-level mosaicism in affected and non affected tissue of a complex CDH patient Gene expression profiling in a mouse model identifies fetal liver- and placenta-derived potential biomarkers for Down Syndrome screening.Functional transcriptome analysis of the postnatal brain of the Ts1Cje mouse model for Down syndrome reveals global disruption of interferon-related molecular networks Noninvasive prenatal testing creates an opportunity for antenatal treatment of Down syndrome.Identification of the translocation breakpoints in the Ts65Dn and Ts1Cje mouse lines: relevance for modeling Down syndrome.Mouse models for Down syndrome-associated developmental cognitive disabilities The use of mouse models for understanding the biology of down syndrome and aging Increased excitability and altered action potential waveform in cerebellar granule neurons of the Ts65Dn mouse model of Down syndrome Sensitized phenotypic screening identifies gene dosage sensitive region on chromosome 11 that predisposes to disease in mice Molecular and cellular alterations in Down syndrome: toward the identification of targets for therapeutics Down syndrome and the molecular pathogenesis resulting from trisomy of human chromosome 21.Stem and progenitor cell dysfunction in human trisomies.Mouse-based genetic modeling and analysis of Down syndrome.Analysis of adult cerebral cortex and hippocampus transcriptomes reveals unique molecular changes in the Ts1Cje mouse model of down syndrome.A Comprehensive Diverse '-omics' Approach to Better Understanding the Molecular Pathomechanisms of Down Syndrome.Rodent models in Down syndrome research: impact and future opportunities.Evidence that increased Kcnj6 gene dose is necessary for deficits in behavior and dentate gyrus synaptic plasticity in the Ts65Dn mouse model of Down syndrome.Aneuploidy causes tissue-specific qualitative changes in global gene expression patterns in maize.Prenatal diagnosis of posterior fossa anomalies: Additional value of chromosomal microarray analysis in fetuses with cerebellar hypoplasia.Restrained Phosphatidylcholine Synthesis in a Cellular Model of Down's Syndrome is Associated with the Overexpression of Dyrk1A.Non-trisomic homeobox gene expression during craniofacial development in the Ts65Dn mouse model of Down syndrome.The fetal brain transcriptome and neonatal behavioral phenotype in the Ts1Cje mouse model of Down syndrome.Lifespan analysis of brain development, gene expression and behavioral phenotypes in the Ts1Cje, Ts65Dn and Dp(16)1/Yey mouse models of Down syndrome.

P2860

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P2860

Gene expression signature of cerebellar hypoplasia in a mouse model of Down syndrome during postnatal development.

http://www.wikidata.org/entity/Q33424071

description

2009 nî lūn-bûn

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2009 թուականի Մարտին հրատարակուած գիտական յօդուած

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2009 թվականի մարտին հրատարակված գիտական հոդված

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2009年の論文

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2009年論文

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2009年論文

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2009年論文

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2009年論文

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2009年論文

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2009年论文

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Fabien Pasteau

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Isabelle Rivals

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Luce Dauphinot

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Ralph Sinkus

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Randal X Moldrich

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Rosine Wehrle

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P2860

Primary and secondary transcriptional effects in the developing human Down syndrome brain and heart

Normal cerebellar development but susceptibility to seizures in mice lacking G protein-coupled, inwardly rectifying K+ channel GIRK2

Monoamine oxidase A and repressor R1 are involved in apoptotic signaling pathway

Distinct human NUMB isoforms regulate differentiation vs. proliferation in the neuronal lineage

Global up-regulation of chromosome 21 gene expression in the developing Down syndrome brain

The utility of Ki-67 and BrdU as proliferative markers of adult neurogenesis

Multiple roles of the DSCR1 (Adapt78 or RCAN1) gene and its protein product calcipressin 1 (or RCAN1) in disease

Chromosome 21 and down syndrome: from genomics to pathophysiology

Neurite arborization and mosaic spacing in the mouse retina require DSCAM.

An open-access long oligonucleotide microarray resource for analysis of the human and mouse transcriptomes.

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Isabelle Dusart

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