ArticleGenes, brain, and behavior2008
Molecular responses of the Ts65Dn and Ts1Cje mouse models of Down syndrome to MK-801.
Article in Genes, brain, and behavior, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 56 citations in OpenAlex.
- Duplication-based genetic dissection of the Down syndrome critical region reveals its complex functional organization.G3 (Bethesda, Md.) · 2026Article
- AKT Hyperphosphorylation and T Cell Exhaustion in Down Syndrome.Frontiers in immunology · 2022Observational
- The Rac-GEF Tiam1 Promotes Dendrite and Synapse Stabilization of Dentate Granule Cells and Restricts Hippocampal-Dependent Memory Functions.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Targeting increased levels of APP in Down syndrome: Posiphen-mediated reductions in APP and its products reverse endosomal phenotypes in the Ts65Dn mouse model.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2021Article
- Quantitative Analysis of Retinal Structure and Function in Two Chromosomally Altered Mouse Models of Down Syndrome.Investigative ophthalmology & visual science · 2020Article
- DYRK1A Protein, A Promising Therapeutic Target to Improve Cognitive Deficits in Down Syndrome.Brain sciences · 2018Review
- In vivo and ex vivo analyses of amyloid toxicity in the Tc1 mouse model of Down syndrome.Journal of psychopharmacology (Oxford, England) · 2018Article
- Phosphoproteomic Alterations of Ionotropic Glutamate Receptors in the Hippocampus of the Ts65Dn Mouse Model of Down Syndrome.Frontiers in molecular neuroscience · 2018Article
- Targeting trisomic treatments: optimizing Dyrk1a inhibition to improve Down syndrome deficits.Molecular genetics & genomic medicine · 2017Review
- Synaptopathies: synaptic dysfunction in neurological disorders - A review from students to students.Journal of neurochemistry · 2016Review
- Pharmacological approaches to improving cognitive function in Down syndrome: current status and considerations.Drug design, development and therapy · 2015Review
- Protein dynamics associated with failed and rescued learning in the Ts65Dn mouse model of Down syndrome.PloS one · 2015Article
- Self-Organizing Feature Maps Identify Proteins Critical to Learning in a Mouse Model of Down Syndrome.PloS one · 2015Article
- Neuropathological role of PI3K/Akt/mTOR axis in Down syndrome brain.Biochimica et biophysica acta · 2014Article
- Unraveling the complexity of neurodegeneration in brains of subjects with Down syndrome: insights from proteomics.Proteomics. Clinical applications · 2014Review
- DYRK1A-mediated phosphorylation of GluN2A at Ser(1048) regulates the surface expression and channel activity of GluN1/GluN2A receptors.Frontiers in cellular neuroscience · 2014Article
- Review
- Protein profiles in Tc1 mice implicate novel pathway perturbations in the Down syndrome brain.Human molecular genetics · 2013Article
- Selective binding of nuclear alpha-synuclein to the PGC1alpha promoter under conditions of oxidative stress may contribute to losses in mitochondrial function: implications for Parkinson's disease.Free radical biology & medicine · 2012Article
- Altered regulation of tau phosphorylation in a mouse model of down syndrome aging.Neurobiology of aging · 2012Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Down syndrome (DS), caused by trisomy of human chromosome 21 (chr21), is the most common genetic cause of intellectual disability. The Ts65Dn mouse model of DS is trisomic for orthologs of 94 chr21-encoded, confirmed protein-coding genes and displays a number of behavioral deficits. Recently, Ts65Dn mice were shown to be hypersensitive to the locomotor stimulatory effects of the high-affinity N-methyl-d-aspartate (NMDA) receptor (NMDAR) channel blocker, MK-801. This is consistent with the functions of several chr21 proteins that are predicted directly or indirectly to impact NMDAR function or NMDAR-mediated signaling. In this study, we show that a second mouse model of DS, the Ts1Cje, which is trisomic for 70 protein-coding genes, is also hypersensitive to MK-801. To investigate the molecular basis for the responses to MK-801, we have measured levels of a subset of chr21 and phosphorylated non-chr21 proteins, in the cortex and hippocampus of Ts65Dn and Ts1Cje mice and euploid controls, with and without treatment with MK-801. We show that in euploid mice, the chr21-encoded proteins, TIAM1 and DYRK1A, and phosphorylation of AKT, ERK1/2 and the transcription factor ELK are involved in the MK-801 response. However, in both Ts65Dn and Ts1Cje mice, levels of phosphorylation are constitutively elevated in naïve, unstimulated mice, and the MK-801-induced changes in TIAM1 and DYRK1A and in phosphorylation are either absent or abnormal, with both genotype and brain-region-specific patterns. These results emphasize the complexities of the pathway perturbations that arise with segmental trisomy.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.