ArticleMammalian genome : official journal of the International Mammalian Genome Society2010
Deficiencies in the region syntenic to human 21q22.3 cause cognitive deficits in mice.
Article in Mammalian genome : official journal of the International Mammalian Genome Society, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 28 citations in OpenAlex.
- Article
- Genetic dissection of down syndrome-associated alterations in APP/amyloid-β biology using mouse models.Scientific reports · 2021Article
- Behavioral Phenotyping for Down Syndrome in Mice.Current protocols in mouse biology · 2020Article
- Rodent models in Down syndrome research: impact and future opportunities.Disease models & mechanisms · 2017Review
- Unraveling the genetic architecture of copy number variants associated with schizophrenia and other neuropsychiatric disorders.Journal of neuroscience research · 2017Review
- Mouse-based genetic modeling and analysis of Down syndrome.British medical bulletin · 2016Review
- Maternal Choline Supplementation: A Potential Prenatal Treatment for Down Syndrome and Alzheimer's Disease.Current Alzheimer research · 2016Article
- RCAN1 links impaired neurotrophin trafficking to aberrant development of the sympathetic nervous system in Down syndrome.Nature communications · 2015Article
- Deletion of the App-Runx1 region in mice models human partial monosomy 21.Disease models & mechanisms · 2015Article
- Dosage of the Abcg1-U2af1 region modifies locomotor and cognitive deficits observed in the Tc1 mouse model of Down syndrome.PloS one · 2015Article
- Cognition and hippocampal plasticity in the mouse is altered by monosomy of a genomic region implicated in Down syndrome.Genetics · 2014Article
- Modeling partial monosomy for human chromosome 21q11.2-q21.1 reveals haploinsufficient genes influencing behavior and fat deposition.PloS one · 2012Article
- Mouse models of aneuploidy.TheScientificWorldJournal · 2012Review
- The telomeric part of the human chromosome 21 from Cstb to Prmt2 is not necessary for the locomotor and short-term memory deficits observed in the Tc1 mouse model of Down syndrome.Behavioural brain research · 2011Article
- Mouse models for Down syndrome-associated developmental cognitive disabilities.Developmental neuroscience · 2011Review
- Down syndrome: from understanding the neurobiology to therapy.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010Review
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Authors and funding
13 authors at 9 institutions in 3 countries.
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Abstract
Copy-number variation in the human genome can be disease-causing or phenotypically neutral. This type of genetic rearrangement associated with human chromosome 21 (Hsa21) underlies partial Monosomy 21 and Trisomy 21. Mental retardation is a major clinical manifestation of partial Monosomy 21. To model this human chromosomal deletion disorder, we have generated novel mouse mutants carrying heterozygous deletions of the 2.3- and 1.1-Mb segments on mouse chromosome 10 (Mmu10) and Mmu17, respectively, which are orthologous to the regions on human 21q22.3, using Cre/loxP-mediated chromosome engineering. Alterations of the transcriptional levels of genes within the deleted intervals reflect gene-dosage effects in the mutant mice. The analysis of cognitive behaviors shows that the mutant mice carrying the deletion on either Mmu10 or Mmu17 are impaired in learning and memory. Therefore, these mutants represent mouse models for Monosomy 21-associated mental retardation, which can serve as a powerful tool to study the molecular mechanism underlying the clinical phenotype and should facilitate efforts to identify the haploinsufficient causative genes.
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