ArticleGenome research2000
The mouse brain transcriptome by SAGE: differences in gene expression between P30 brains of the partial trisomy 16 mouse model of Down syndrome (Ts65Dn) and normals.
Article in Genome research, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.
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Who cites it
35 citing papers in PubMed, 1 synthesis or guideline pooled it, 94 citations in OpenAlex.
- Meta-analysis of heterogeneous Down Syndrome data reveals consistent genome-wide dosage effects related to neurological processes.BMC genomics · 2011Pooled it
- Article
- Glutamatergic synaptic deficits in the prefrontal cortex of the Ts65Dn mouse model for Down syndrome.Frontiers in neuroscience · 2023Article
- Restoring neuronal chloride homeostasis with anti-NKCC1 gene therapy rescues cognitive deficits in a mouse model of Down syndrome.Molecular therapy : the journal of the American Society of Gene Therapy · 2021Article
- Single cell transcriptome in aneuploidies reveals mechanisms of gene dosage imbalance.Nature communications · 2019Article
- Maternal Choline Supplementation Alters Basal Forebrain Cholinergic Neuron Gene Expression in the Ts65Dn Mouse Model of Down Syndrome.Developmental neurobiology · 2019Article
- Isolation and RNA Extraction of Neurons, Macrophages and Microglia from Larval Zebrafish Brains.Journal of visualized experiments : JoVE · 2018Article
- Proteomic analysis of six- and twelve-month hippocampus and cerebellum in a murine Down syndrome model.Neurobiology of aging · 2018Article
- Candidate gene analysis for Alzheimer's disease in adults with Down syndrome.Neurobiology of aging · 2017Article
- A Comprehensive Diverse '-omics' Approach to Better Understanding the Molecular Pathomechanisms of Down Syndrome.Brain sciences · 2017Review
- Sex differences in the cholinergic basal forebrain in the Ts65Dn mouse model of Down syndrome and Alzheimer's disease.Brain pathology (Zurich, Switzerland) · 2014Article
- The intellectual disability of trisomy 21: differences in gene expression in a case series of patients with lower and higher IQ.European journal of human genetics : EJHG · 2013Article
- Genomics and proteomics in solving brain complexity.Molecular bioSystems · 2013Review
- Article
- Down syndrome: the brain in trisomic mode.Nature reviews. Neuroscience · 2012Review
- Abnormal microRNA expression in Ts65Dn hippocampus and whole blood: contributions to Down syndrome phenotypes.Developmental neuroscience · 2011Article
- A serial analysis of gene expression profile of the Alzheimer's disease Tg2576 mouse model.Neurotoxicity research · 2010Article
- A new mouse model for the trisomy of the Abcg1-U2af1 region reveals the complexity of the combinatorial genetic code of down syndrome.Human molecular genetics · 2009Article
- Molecular genetic analysis of Down syndrome.Human genetics · 2009Review
- Genotype-phenotype correlations in Down syndrome identified by array CGH in 30 cases of partial trisomy and partial monosomy chromosome 21.European journal of human genetics : EJHG · 2009Article
Corrections and comments
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Authors and funding
12 authors at 1 institution in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Trisomy 21, or Down syndrome (DS), is the most common genetic cause of mental retardation. Changes in the neuropathology, neurochemistry, neurophysiology, and neuropharmacology of DS patients' brains indicate that there is probably abnormal development and maintenance of central nervous system structure and function. The segmental trisomy mouse (Ts65Dn) is a model of DS that shows analogous neurobehavioral defects. We have studied the global gene expression profiles of normal and Ts65Dn male and normal female mice brains (P30) using the serial analysis of gene expression (SAGE) technique. From the combined sample we collected a total of 152,791 RNA tags and observed 45,856 unique tags in the mouse brain transcriptome. There are 14 ribosomal protein genes (nine under expressed) among the 330 statistically significant differences between normal male and Ts65Dn male brains, which possibly implies abnormal ribosomal biogenesis in the development and maintenance of DS phenotypes. This study contributes to the establishment of a mouse brain transcriptome and provides the first overall analysis of the differences in gene expression in aneuploid versus normal mammalian brain cells.
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