ArticleGenome research2002
Comparative genomic sequence analysis of the human chromosome 21 Down syndrome critical region.
Article in Genome research, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 52 citations in OpenAlex.
- Enhanced GIRK2 channel signaling in Down syndrome: A feasible role in the development of abnormal nascent neural circuits.Frontiers in genetics · 2022Review
- Genome-Wide Association Study Identifies a Susceptibility Locus for Comitant Esotropia and Suggests a Parent-of-Origin Effect.Investigative ophthalmology & visual science · 2018Article
- DYRK1A-mediated Cyclin D1 Degradation in Neural Stem Cells Contributes to the Neurogenic Cortical Defects in Down Syndrome.EBioMedicine · 2015Article
- Behavioral and Genetic Evidence for GIRK Channels in the CNS: Role in Physiology, Pathophysiology, and Drug Addiction.International review of neurobiology · 2015Review
- DSCR9 gene simultaneous expression in placental, testicular and renal tissues from baboon (Papio hamadryas).BMC research notes · 2012Article
- Working memory in the aged Ts65Dn mouse, a model for Down syndrome.Behavioural brain research · 2012Article
- The unipolar brush cell: a remarkable neuron finally receiving deserved attention.Brain research reviews · 2011Review
- The arrestin fold: variations on a theme.Current genomics · 2009Article
- Abnormal expression of the G-protein-activated inwardly rectifying potassium channel 2 (GIRK2) in hippocampus, frontal cortex, and substantia nigra of Ts65Dn mouse: a model of Down syndrome.The Journal of comparative neurology · 2006Article
- Leveraging the mouse genome for gene prediction in human: from whole-genome shotgun reads to a global synteny map.Genome research · 2003Article
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Authors and funding
8 authors at 1 institution in 3 countries.
Funding
Abstract
Comprehensive knowledge of the gene content of human chromosome 21 (HSA21) is essential for understanding the etiology of Down syndrome (DS). Here we report the largest comparison of finished mouse and human sequence to date for a 1.35-Mb region of mouse chromosome 16 (MMU16) that corresponds to human chromosome 21q22.2. This includes a portion of the commonly described "DS critical region," thought to contain a gene or genes whose dosage imbalance contributes to a number of phenotypes associated with DS. We used comparative sequence analysis to construct a DNA feature map of this region that includes all known genes, plus 144 conserved sequences > or =100 bp long that show > or =80% identity between mouse and human but do not match known exons. Twenty of these have matches to expressed sequence tag and cDNA databases, indicating that they may be transcribed sequences from chromosome 21. Eight putative CpG islands are found at conserved positions. Models for two human genes, DSCR4 and DSCR8, are not supported by conserved sequence, and close examination indicates that low-level transcripts from these loci are unlikely to encode proteins. Gene prediction programs give different results when used to analyze the well-conserved regions between mouse and human sequences. Our findings have implications for evolution and for modeling the genetic basis of DS in mice.
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Registered trials
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.