| Resource No. |
nbio175 |
| Strain name |
IRD2 |
| Strain Nomenclature |
|
| Common name/Synonyms |
ICR-derived retinal dysfunction 2 mice |
| Strain types |
outbred |
| Background strain |
|
| Institution |
Takeda Pharmaceutical Co., Ltd. |
| Developer |
Makoto Miyamoto |
| Depositor |
Makoto Miyamoto |
| Conditions of distribution |
In publishing the research results obtained by use of the biological resource, a citation of the following literature (ref. 1, 2, 3) designated by the depositor is requested. The recipient agrees that LARB informs the depositor of recipient organization, recipient name and the specific research purpose. :contact us |
| Animal Health Report |
|
| Strain description |
IRD2 mice become spontaneous inheritable rod dysfunction, and they are observed late-onset progressive retinal degeneration. It's considered that the cause of rod dysfunction is the deletion of Trα protein caused by nonsense mutation of Gnat1 gene. The rod function is normal. It's considered that this strain is useful for the research of inheritable retinal disease. This strain is derived from Crj:CD-1(ICR). It's possible to supply IRD1 mice observed rod and cone dysfunction. |
| Reference(s) |
- Miyamoto M, Aoki M, Sugimoto S, Kawasaki K, and Imai R. (2010) IRD1 and IRD2 mice, naturally occurring models of hereditary retinal dysfunction, show late-onset and progressive retinal degeneration. Curr Eye Res 35(2):137-45. [PMID:20136424]
- Miyamoto M, Aoki M, Hirai K, Sugimoto S, Kawasaki K, and Imai R. (2010) A nonsense mutation in Gnat1, encoding the alpha subunit of rod transducin, in spontaneous mouse models of retinal dysfunction. Exp Eye Res 90(1):63-9. [PMID:19766629]
- Miyamoto M, Imai R, Sugimoto S, Aoki M, Nagai H, and Ando T. (2006) Visual electrophysiological features of two naturally occurring mouse models with retinal dysfunction. Curr Eye Res 31(4):329-35. [PMID:16603466]
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