ArticleBMC genomics2014
Functional transcriptome analysis of the postnatal brain of the Ts1Cje mouse model for Down syndrome reveals global disruption of interferon-related molecular networks.
Article in BMC genomics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 2 of them syntheses that pooled it.
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Who cites it
38 citing papers in PubMed, 2 syntheses or guidelines pooled it, 69 citations in OpenAlex.
- Meta-analysis of transcriptomic data reveals clusters of consistently deregulated gene and disease ontologies in Down syndrome.PLoS computational biology · 2021Pooled it
- Genome-wide DNA methylation meta-analysis in the brains of suicide completers.Translational psychiatry · 2020Pooled it
- Trial
- Review
- Dissection of a Down syndrome-associated trisomy to separate the gene dosage-dependent and -independent effects of an extra chromosome.Human molecular genetics · 2023Article
- Paxbp1 is indispensable for the survival of CD4 and CD8 double-positive thymocytes.Frontiers in immunology · 2023Article
- Shaking up the silence: consequences of HMGN1 antagonizing PRC2 in the Down syndrome brain.Epigenetics & chromatin · 2022Review
- Ts66Yah, a mouse model of Down syndrome with improved construct and face validity.Disease models & mechanisms · 2022Article
- Lamivudine, a reverse transcriptase inhibitor, rescues cognitive deficits in a mouse model of down syndrome.Journal of cellular and molecular medicine · 2022Article
- The accumulation of copper in the brain of Down syndrome promotes oxidative stress: possible mechanism underlying cognitive impairment.Journal of clinical biochemistry and nutrition · 2022Article
- The Vulnerability of the Developing Brain: Analysis of Highly Expressed Genes in Infant C57BL/6 Mouse Hippocampus in Relation to Phenotypic Annotation Derived From Mutational Studies.Bioinformatics and biology insights · 2022Article
- Multi-influential genetic interactions alter behaviour and cognition through six main biological cascades in Down syndrome mouse models.Human molecular genetics · 2021Article
- Network analysis of Down syndrome and SARS-CoV-2 identifies risk and protective factors for COVID-19.Scientific reports · 2021Article
- Kisspeptin Influences the Reproductive Axis and Circulating Levels of microRNAs in Senegalese Sole.International journal of molecular sciences · 2020Article
- Quantitative Proteomics Reveals Docosahexaenoic Acid-Mediated Neuroprotective Effects in Lipopolysaccharide-Stimulated Microglial Cells.Journal of proteome research · 2020Article
- Biological Functions of HMGN Chromosomal Proteins.International journal of molecular sciences · 2020Review
- Autoimmune Mechanisms of Interferon Hypersensitivity and Neurodegenerative Diseases: Down Syndrome.Autoimmune diseases · 2020Article
- Phenotype microarrays reveal metabolic dysregulations of neurospheres derived from embryonic Ts1Cje mouse model of Down syndrome.PloS one · 2020Article
- Genetic and epigenetic pathways in Down syndrome: Insights to the brain and immune system from humans and mouse models.Progress in brain research · 2020Review
- Expression Profiling of Notch Signalling Pathway and Gamma-Secretase Activity in the Brain of Ts1Cje Mouse Model of Down Syndrome.Journal of molecular neuroscience : MN · 2019Article
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe Ts1Cje mouse model of Down syndrome (DS) has partial triplication of mouse chromosome 16 (MMU16), which is partially homologous to human chromosome 21. These mice develop various neuropathological features identified in DS individuals. We analysed the effect of partial triplication of the MMU16 segment on global gene expression in the cerebral cortex, cerebellum and hippocampus of Ts1Cje mice at 4 time-points: postnatal day (P)1, P15, P30 and P84.
resultsGene expression profiling identified a total of 317 differentially expressed genes (DEGs), selected from various spatiotemporal comparisons, between Ts1Cje and disomic mice. A total of 201 DEGs were identified from the cerebellum, 129 from the hippocampus and 40 from the cerebral cortex. Of these, only 18 DEGs were identified as common to all three brain regions and 15 were located in the triplicated segment. We validated 8 selected DEGs from the cerebral cortex (Brwd1, Donson, Erdr1, Ifnar1, Itgb8, Itsn1, Mrps6 and Tmem50b), 18 DEGs from the cerebellum (Atp5o, Brwd1, Donson, Dopey2, Erdr1, Hmgn1, Ifnar1, Ifnar2, Ifngr2, Itgb8, Itsn1, Mrps6, Paxbp1, Son, Stat1, Tbata, Tmem50b and Wrb) and 11 DEGs from the hippocampus (Atp5o, Brwd1, Cbr1, Donson, Erdr1, Itgb8, Itsn1, Morc3, Son, Tmem50b and Wrb). Functional clustering analysis of the 317 DEGs identified interferon-related signal transduction as the most significantly dysregulated pathway in Ts1Cje postnatal brain development. RT-qPCR and western blotting analysis showed both Ifnar1 and Stat1 were over-expressed in P84 Ts1Cje cerebral cortex and cerebellum as compared to wild type littermates.
conclusionsThese findings suggest over-expression of interferon receptor may lead to over-stimulation of Jak-Stat signaling pathway which may contribute to the neuropathology in Ts1Cje or DS brain. The role of interferon mediated activation or inhibition of signal transduction including Jak-Stat signaling pathway has been well characterized in various biological processes and disease models including DS but information pertaining to the role of this pathway in the development and function of the Ts1Cje or DS brain remains scarce and warrants further investigation.
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