ArticleAmerican journal of medical genetics. Part A2009
Complex contributions of Ets2 to craniofacial and thymus phenotypes of trisomic "Down syndrome" mice.
Article in American journal of medical genetics. Part A, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 32 citations in OpenAlex.
- p75 neurotrophin receptor regulates craniofacial growth and morphology in postnatal development.Frontiers in cell and developmental biology · 2025Article
- A murine model of hnRNPH2-related neurodevelopmental disorder reveals a mechanism for genetic compensation by Hnrnph1.The Journal of clinical investigation · 2023Article
- Overexpression screen of chromosome 21 genes reveals modulators of Sonic hedgehog signaling relevant to Down syndrome.Disease models & mechanisms · 2023Article
- Green Tea Catechins Modulate Skeletal Development with Effects Dependent on Dose, Time, and Structure in a down Syndrome Mouse Model.Nutrients · 2022Article
- Unilateral Loss of Maxillary Molars in Young Mice Leads to Bilateral Condylar Adaptation and Degenerative Disease.JBMR plus · 2022Article
- A landmark-free morphometrics pipeline for high-resolution phenotyping: application to a mouse model of Down syndrome.Development (Cambridge, England) · 2021Article
- Influence of allelic differences in Down syndrome.Progress in brain research · 2020Review
- Double deletion of Panx1 and Panx3 affects skin and bone but not hearing.Journal of molecular medicine (Berlin, Germany) · 2019Article
- Gene expression in the phenotypically plastic Arctic charr (Salvelinus alpinus): A focus on growth and ossification at early stages of development.Evolution & development · 2019Article
- Altered Neocortical Gene Expression, Brain Overgrowth and Functional Over-Connectivity in Chd8 Haploinsufficient Mice.Cerebral cortex (New York, N.Y. : 1991) · 2018Article
- Targeting trisomic treatments: optimizing Dyrk1a inhibition to improve Down syndrome deficits.Molecular genetics & genomic medicine · 2017Review
- Trans-acting epigenetic effects of chromosomal aneuploidies: lessons from Down syndrome and mouse models.Epigenomics · 2017Review
- Influence of prenatal EGCG treatment and Dyrk1a dosage reduction on craniofacial features associated with Down syndrome.Human molecular genetics · 2016Article
- Stem and progenitor cell dysfunction in human trisomies.EMBO reports · 2015Review
- Identification of Chiari Type I Malformation subtypes using whole genome expression profiles and cranial base morphometrics.BMC medical genomics · 2014Article
- The use of mouse models for understanding the biology of down syndrome and aging.Current gerontology and geriatrics research · 2012Article
- Trisomic and allelic differences influence phenotypic variability during development of Down syndrome mice.Genetics · 2011Article
- Identification of the translocation breakpoints in the Ts65Dn and Ts1Cje mouse lines: relevance for modeling Down syndrome.Mammalian genome : official journal of the International Mammalian Genome Society · 2011Article
- Down syndrome: searching for the genetic culprits.Disease models & mechanisms · 2011Review
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Ts65Dn mice have segmental trisomy for orthologs of about half of the genes on human chromosome 21, including Ets2. These mice develop anomalies of the cranial skeleton and thymus that parallel those in Down syndrome. Overexpression of the Ets2 transcription factor gene was posited to be sufficient to produce these craniofacial and thymus deficits in transgenic mice that constitutively overexpress a processed Ets2 transcript under a promiscuous promoter [Sumarsono et al. (1996); Nature 379:534-537; Wolvetang et al. (2003); Hum Mol Genet 12:247-255]. Evaluation of trisomic mice with varying copy numbers of a properly regulated Ets2 gene indicated increased dosage of Ets2 was not sufficient to produce effects on thymus and most of the cranial anomalies seen in Ts65Dn mice. However, mesoderm-derived cranial skeletal elements are significantly more affected in Ts65Dn, Ets2(+/-) mice compared to Ts65Dn littermates suggesting a differential interaction of Ets2-related processes with mesoderm-derived and neural crest-derived formative tissues. Our results support the growing evidence for interactions among multiple genes contributing to developmental perturbations resulting in variation in complex Down syndrome phenotypes.
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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.