ArticleMammalian genome : official journal of the International Mammalian Genome Society2011
Molecular characterization of the translocation breakpoints in the Down syndrome mouse model Ts65Dn.
Article in Mammalian genome : official journal of the International Mammalian Genome Society, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 123 papers.
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Who cites it
123 citing papers in PubMed, 188 citations in OpenAlex.
- Article
- Gene dosage imbalance disrupts systemic metabolism in the Dp16 Down syndrome mouse model.eLife · 2026Article
- A Researcher's guide to rodent models of Down syndrome: Recent insights and translational perspectives.STAR protocols · 2026Review
- Sex-specific developmental phenotypes and their response to neonatalbioRxiv : the preprint server for biology · 2026Article
- Genetic analysis of triplicated genes affecting sex-specific skeletal deficits in Down syndrome model mice.G3 (Bethesda, Md.) · 2026Article
- The cholinergic system exerts opposing effects on memory at different stages of disease progression in Alzheimer's and Down syndrome model systems.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Gene dosage imbalance disrupts systemic metabolism in the Dp16 Down syndrome mouse model.bioRxiv : the preprint server for biology · 2026Article
- Increased dendritic inhibition of dentate gyrus granule cells in a mouse model of Down syndrome.Frontiers in cellular neuroscience · 2026Article
- Opposing interictal dynamics in Alzheimer's disease and epilepsy.Progress in neurobiology · 2026Article
- Genetic analysis of triplicated genes affecting sex-specific skeletal deficits in Down syndrome model mice.bioRxiv : the preprint server for biology · 2025Article
- Dysregulation of astrocyte-secreted pleiotrophin contributes to neuronal structural and functional deficits in Down syndrome.Cell reports · 2025Article
- Cardiopulmonary and Immune Alterations in the Ts65Dn Mouse Model of Down Syndrome and Modulation by Epigallocatechin-3-Gallate-Enriched Green Tea Extract.Pharmaceutics · 2025Article
- Disrupted Neurogenesis from Basal Intermediate Precursor Cells Alters the Postnatal Neocortex in the TcMAC21 Mouse Model of Down Syndrome.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Assessing the Benefit of Dietary Choline Supplementation Throughout Adulthood in the Ts65Dn Mouse Model of Down Syndrome.Nutrients · 2024Article
- Sex-specific trisomic Dyrk1a-related skeletal phenotypes during development in a Down syndrome model.Disease models & mechanisms · 2024Article
- Aging exacerbates oxidative stress and liver fibrosis in an animal model of Down Syndrome.Aging · 2024Article
- Comparative analysis of craniofacial shape in two mouse models of Down syndrome: Ts65Dn and TcMAC21.Journal of anatomy · 2024Article
- Sex specific emergence of trisomicbioRxiv : the preprint server for biology · 2024Article
- Altered Brain Cholesterol Machinery in a Down Syndrome Mouse Model: A Possible Common Feature with Alzheimer's Disease.Antioxidants (Basel, Switzerland) · 2024Article
- Article
63 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issuedGilbert, Griffith T [corrected to Gilbert, Griffith J]
Authors and funding
11 authors at 5 institutions in 1 country.
Funding
Abstract
Ts65Dn is a mouse model of Down syndrome: a syndrome that results from chromosome (Chr) 21 trisomy and is associated with congenital defects, cognitive impairment, and ultimately Alzheimer's disease. Ts65Dn mice have segmental trisomy for distal mouse Chr 16, a region sharing conserved synteny with human Chr 21. As a result, this strain harbors three copies of over half of the human Chr 21 orthologs. The trisomic segment of Chr 16 is present as a translocation chromosome (Mmu17(16)), with breakpoints that have not been defined previously. To molecularly characterize the Chrs 16 and 17 breakpoints on the translocation chromosome in Ts65Dn mice, we used a selective enrichment and high-throughput paired-end sequencing approach. Analysis of paired-end reads flanking the Chr 16, Chr 17 junction on Mmu17(16) and de novo assembly of the reads directly spanning the junction provided the precise locations of the Chrs 16 and 17 breakpoints at 84,351,351 and 9,426,822 bp, respectively. These data provide the basis for low-cost, highly efficient genotyping of Ts65Dn mice. More importantly, these data provide, for the first time, complete characterization of gene dosage in Ts65Dn mice.
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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.