Genetic modifiers of rodent animal models: the role in cataractogenesis
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- Wada Kenta
- Faculty of Bioindustry, Tokyo University of Agriculture, 196 Yasaka, Abashiri, Hokkaido 099-2493, Japan Mammalian Genetics Project, Department of Genome Medicine, Tokyo Metropolitan Institute of Medical Science, 2–1–6 Kamikitazawa, Setagaya-ku, Tokyo 156-8506, Japan
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- Yasuda Shumpei P.
- Mammalian Genetics Project, Department of Genome Medicine, Tokyo Metropolitan Institute of Medical Science, 2–1–6 Kamikitazawa, Setagaya-ku, Tokyo 156-8506, Japan
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- Kikkawa Yoshiaki
- Mammalian Genetics Project, Department of Genome Medicine, Tokyo Metropolitan Institute of Medical Science, 2–1–6 Kamikitazawa, Setagaya-ku, Tokyo 156-8506, Japan
Bibliographic Information
- Other Title
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- Young Investigator Award : Genetic modifiers of rodent animal models : the role in cataractogenesi
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Abstract
<p>Visual impairment leads to a decrease in quality of life. Cataract is the most commonly observed ocular disease in humans that causes vision disorders. The risk factors associated with cataract development include aging, infections, eye injuries, environmental causes, such as radiation and exposure to ultraviolet rays in sunlight, and genetic mutations. Additionally, several cataract patients display phenotypic heterogeneity, suggesting the role of genetic modifiers in the modulation of severity and onset time of cataractogenesis. However, the genetic modifiers associated with cataract have not been identified in humans yet. In contrast, the identification and mapping of genetic modifiers have been successfully carried out in mice and rats. In this review, we focus on the genetic modifiers of cataract in the rodent models.</p>
Journal
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- Experimental Animals
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Experimental Animals 68 (4), 397-406, 2019
Japanese Association for Laboratory Animal Science
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Details 詳細情報について
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- CRID
- 1390845702312051968
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- NII Article ID
- 130007742219
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- NII Book ID
- AA11032321
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- ISSN
- 18817122
- 00075124
- 13411357
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- NDL BIB ID
- 030066121
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- PubMed
- 31105106
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- Text Lang
- en
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- Data Source
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- JaLC
- NDL
- Crossref
- PubMed
- CiNii Articles
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- Abstract License Flag
- Disallowed