Ts1Cje, a partial trisomy 16 mouse model for Down syndrome, exhibits learning and behavioral abnormalities

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Developmental molecular and functional cerebellar alterations induced by PCP4/PEP19 overexpression: Implications for Down syndrome

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Gene Expression Profiling in a Mouse Model Identifies Fetal Liver- and Placenta-Derived Potential Biomarkers for Down Syndrome Screening

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Quantitative Proteomics Characterization of a Mouse Embryonic Stem Cell Model of Down Syndrome

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Comparative proteomic profiling reveals aberrant cell proliferation in the brain of embryonic Ts1Cje, a mouse model of Down syndrome

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Tissue-specific overexpression of the HSA21 gene GABPα: implications for DS

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Copper accumulation in the brain causes the elevation of oxidative stress and less anxious behavior in Ts1Cje mice, a model of Down syndrome

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A third copy of the Down syndrome cell adhesion molecule (Dscam) causes synaptic and locomotor dysfunction in Drosophila

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A novel mouse model for Down syndrome that harbor a single copy of human artificial chromosome (HAC) carrying a limited number of genes from human chromosome 21

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Gene and protein expression profiles of JAK-STAT signalling pathway in the developing brain of the Ts1Cje down syndrome mouse model

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Behavioral Phenotyping for Down Syndrome in Mice

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Human chromosome 21q22.2-qter carries a gene(s) responsible for downregulation of mlc2a and PEBP in Down syndrome model mice

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Molecular aspects of Down syndrome.

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Triple play of DYRK1A kinase in cortical progenitor cells of Trisomy 21

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GIRK Channels

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Suprachiasmatic lesions restore object recognition in down syndrome model mice

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An extra human chromosome 21 reduces mlc-2a expression in chimeric mice and Down syndrome

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Surveying the Down syndrome mouse model resource identifies critical regions responsible for chronic otitis media

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Neocortical neuronal production and maturation defects in the TcMAC21 mouse model of Down syndrome

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Shaking up the silence: consequences of HMGN1 antagonizing PRC2 in the Down syndrome brain

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Acetylcholinesterase as a window onto stress responses

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A new mouse model for Down syndrome

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Specific age-related molecular alterations in the cerebellum of Down syndrome mouse models

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Perinatal Natural History of the Ts1Cje Mouse Model of Down Syndrome: Growth Restriction, Early Mortality, Heart Defects, and Delayed Development

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Genetic analysis of Down syndrome facilitated by mouse chromosome engineering

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Perturbation of the immune cells and prenatal neurogenesis by the triplication of the Erg gene in mouse models of Down syndrome

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Impairment of spatial memory accuracy improved by Cbr1 copy number resumption and GABAB receptor-dependent enhancement of synaptic inhibition in Down syndrome model mice

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Signalling pathways contributing to learning and memory deficits in the Ts65Dn mouse model of Down syndrome

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Long-range chromosomal engineering is more efficient in vitro than in vitro

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RGS Proteins Maintain Robustness of GPCR-GIRK Coupling by Selective Stimulation of the G Protein Subunit Gα o

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Molecular misreading of genes in Down syndrome as a model for the Alzheimer type of neurodegeneration

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Influence of allelic differences in Down syndrome

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Trisomie 21 : 50 ans entre médecine et science

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Genes Associated with Disturbed Cerebral Neurogenesis in the Embryonic Brain of Mouse Models of Down Syndrome

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Coat Color-Facilitated Efficient Generation and Analysis of a Mouse Model of Down Syndrome Triplicated for All Human Chromosome 21 Orthologous Regions

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Astrocytic Alterations and Dysfunction in Down Syndrome: Focus on Neurogenesis, Synaptogenesis, and Neural Circuits Formation

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Brain plasticity and environmental enrichment in Ts65Dn mice, an animal model for Down syndrome

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CPEB1 is overexpressed in neurons derived from Down syndrome IPSCs and in the hippocampus of the mouse model Ts1Cje

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Phenotype microarrays reveal metabolic dysregulations of neurospheres derived from embryonic Ts1Cje mouse model of Down syndrome

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Ripply3 overdosage induces mid-face shortening through Tbx1 downregulation in Down syndrome models

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In and out: Benchmarking in vitro, in vivo, ex vivo, and xenografting approaches for an integrative brain disease modeling pipeline

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Controlled Somatic and Germline Copy Number Variation in the Mouse Model

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Activity-Dependent Dysfunction in Visual and Olfactory Sensory Systems in Mouse Models of Down Syndrome

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Animal models of Down syndrome

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Decrease in the T-box1 gene expression in embryonic brain and adult hippocampus of down syndrome mouse models.

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Novel insights from fetal and placental phenotyping in 3 mouse models of Down syndrome

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Expression Profiling of Notch Signalling Pathway and Gamma-Secretase Activity in the Brain of Ts1Cje Mouse Model of Down Syndrome

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Knockdown of Myo-Inositol Transporter SMIT1 Normalizes Cholinergic and Glutamatergic Function in an Immortalized Cell Line Established from the Cerebral Cortex of a Trisomy 16 Fetal Mouse, an Animal Model of Human Trisomy 21 (Down Syndrome)

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Effects of a Tripeptide on Mitogen-Activated Protein Kinase and Glycogen Synthase Kinase Activation in a Cell Line Derived from the Foetal Hippocampus of a Trisomy 16 Mouse: an Animal Model of Down Syndrome

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Nonlinear Optics in Doped Silica Glass Integrated Waveguide Structures

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Molecular Pathways of Down Syndrome Critical Region Genes

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Reduced REST Expression in Neural Progenitor Cells, Adult Cortex, and Impaired REST Nuclear Translocation in the Prefrontal Cortex of Ts1Cje Mouse Model of Down Syndrome

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Structural insights in the permeation mechanism of an activated GIRK2 channel

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Combinatorial Gene Effects on the Neural Progenitor Pool in Down Syndrome

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Down Syndrome: A Complex and Interactive Genetic Disorder

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Genetic Dissection of Region Associated with Behavioral Abnormalities in Mouse Models for Down Syndrome

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A behavioral assessment of Ts65Dn mice: a putative Down syndrome model

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Ts1Cje mouse model for Down syndrome research

Ling, K. H. (2015) · Universiti Putra Malaysia Institutional Repository (Universiti Putra Malaysia)

A mouse model for Down syndrome exhibits learning and behaviour deficits [see comments]

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Ts1Cje Down syndrome model mice exhibit environmental stimuli-triggered locomotor hyperactivity and sociability concurrent with increased flux through central dopamine and serotonin metabolism

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