ArticleGenome research2002
Generation and comparative analysis of approximately 3.3 Mb of mouse genomic sequence orthologous to the region of human chromosome 7q11.23 implicated in Williams syndrome.
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 29 papers.
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29 citing papers in PubMed, 77 citations in OpenAlex.
- Modeling Williams syndrome from a neurodevelopmental perspective: recent advances, model-based translational insights and future directions.World journal of pediatrics : WJP · 2026Review
- A Del(5PNAS nexus · 2025Article
- Conserved Noncoding Elements Evolve Around the Same Genes Throughout Metazoan Evolution.Genome biology and evolution · 2024Article
- Reactive Oxygen Species and Oxidative Stress in the Pathogenesis and Progression of Genetic Diseases of the Connective Tissue.Antioxidants (Basel, Switzerland) · 2020Review
- The other side of the coin: Hypersociability.Genes, brain, and behavior · 2019Review
- Loss of WSTF results in spontaneous fluctuations of heterochromatin formation and resolution, combined with substantial changes to gene expression.BMC genomics · 2013Article
- Autistic disorder in patients with Williams-Beuren syndrome: a reconsideration of the Williams-Beuren syndrome phenotype.PloS one · 2012Article
- Genetic modifiers of cardiovascular phenotype caused by elastin haploinsufficiency act by extrinsic noncomplementation.The Journal of biological chemistry · 2011Article
- Conserved and non-conserved enhancers direct tissue specific transcription in ancient germ layer specific developmental control genes.BMC developmental biology · 2011Article
- Using transcription modules to identify expression clusters perturbed in Williams-Beuren syndrome.PLoS computational biology · 2011Article
- Induced chromosome deletion in a Williams-Beuren syndrome mouse model causes cardiovascular abnormalities.Journal of vascular research · 2011Article
- Expression of the transcription factor, TFII-I, during post-implantation mouse embryonic development.BMC research notes · 2010Article
- Gene expression of NMDA receptor subunits in the cerebellum of elderly patients with schizophrenia.European archives of psychiatry and clinical neuroscience · 2010Article
- Induced chromosome deletions cause hypersociability and other features of Williams-Beuren syndrome in mice.EMBO molecular medicine · 2009Article
- More than the sum of its parts: new mouse models for dissecting the genetic complexities of Williams-Beuren syndrome.EMBO molecular medicine · 2009Article
- Williams-Beuren syndrome TRIM50 encodes an E3 ubiquitin ligase.European journal of human genetics : EJHG · 2008Article
- Analysis of segmental duplications reveals a distinct pattern of continuation-of-synteny between human and mouse genomes.Human genetics · 2007Article
- Human-zebrafish non-coding conserved elements act in vivo to regulate transcription.Nucleic acids research · 2005Article
- An intermediate grade of finished genomic sequence suitable for comparative analyses.Genome research · 2004Article
- Genome annotation of a 1.5 Mb region of human chromosome 6q23 encompassing a quantitative trait locus for fetal hemoglobin expression in adults.BMC genomics · 2004Article
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Authors and funding
16 authors at 1 institution in 1 country.
Funding
Abstract
Williams syndrome is a complex developmental disorder that results from the heterozygous deletion of a approximately 1.6-Mb segment of human chromosome 7q11.23. These deletions are mediated by large (approximately 300 kb) duplicated blocks of DNA of near-identical sequence. Previously, we showed that the orthologous region of the mouse genome is devoid of such duplicated segments. Here, we extend our studies to include the generation of approximately 3.3 Mb of genomic sequence from the mouse Williams syndrome region, of which just over 1.4 Mb is finished to high accuracy. Comparative analyses of the mouse and human sequences within and immediately flanking the interval commonly deleted in Williams syndrome have facilitated the identification of nine previously unreported genes, provided detailed sequence-based information regarding 30 genes residing in the region, and revealed a number of potentially interesting conserved noncoding sequences. Finally, to facilitate comparative sequence analysis, we implemented several enhancements to the program, including the addition of links from annotated features within a generated percent-identity plot to specific records in public databases. Taken together, the results reported here provide an important comparative sequence resource that should catalyze additional studies of Williams syndrome, including those that aim to characterize genes within the commonly deleted interval and to develop mouse models of the disorder.
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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.