ArticleTransgenic research2005
Transgenic expression of CECR1 adenosine deaminase in mice results in abnormal development of heart and kidney.
Article in Transgenic research, 2005. 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, 27 citations in OpenAlex.
- Decoding variants of uncertain significance in systemic autoinflammatory diseases.Nature reviews. Rheumatology · 2026Review
- Article
- Monogenic autoinflammatory disease-associated cardiac damage.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023Review
- Adenosine deaminase 2 produced by infiltrative monocytes promotes liver fibrosis in nonalcoholic fatty liver disease.Cell reports · 2021Article
- Article
- An in vivo RNAi screen uncovers the role of AdoR signaling and adenosine deaminase in controlling intestinal stem cell activity.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Deficiency of Adenosine Deaminase 2 (DADA2): Updates on the Phenotype, Genetics, Pathogenesis, and Treatment.Journal of clinical immunology · 2018Review
- Congenital Heart Defects and Ciliopathies Associated With Renal Phenotypes.Frontiers in pediatrics · 2018Review
- New players driving inflammation in monogenic autoinflammatory diseases.Nature reviews. Rheumatology · 2015Review
- Rare DNA copy number variants in cardiovascular malformations with extracardiac abnormalities.European journal of human genetics : EJHG · 2013Article
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cat eye syndrome is a rare developmental defect associated with duplication of chromosome 22q11. The patients demonstrate specific abnormalities of heart, kidney, and eye. Here we attempted to produce a model for this defect by expressing CECR1 adenosine deaminase, a gene duplicated in cat eye syndrome patients, in mice. The transgenic mice expressed CECR1 under the control of either beta-actin promoter for ubiquitous expression or myosin heavy chain for heart-specific expression. The transgenics expressing CECR1 in the heart demonstrated high rate of embryonic and neonatal lethality. The mice from all the lines examined showed enlargement of the heart. Abnormalities of the kidney and eye were also detected in mice expressing CECR1 under control of the actin promoter.
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Registered trials
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