Genetically modified rat that expresses an F54L Txn1 mutant
AssigneesIori Ohmori, Mamoru Ouchida, Tomoji Mashimo, Hamamatsu Photonics K.K.
InventorsIori Ohmori, Mamoru Ouchida, Tomoji Mashimo
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Abstract
Provided is a nonhuman animal model that is obtained by modifying a gene encoding thioredoxin and useful as a disease model of aging, kidney diseases, cardiovascular diseases, hypertension, aortic dissection, chronic obstructive lung disease, age-dependent epilepsy, abnormality of lipid metabolism, anemia, osteoporosis, abnormal immunity, etc. These variety of phenotypes are caused by the fact that a modification of a gene encoding thioredoxin induces hypofunction of thioredoxin expressed in multiple organs throughout the body. The gene encoding thioredoxin is a gene selected from among TXN, TRX, TRX1, RRDX, Txn1, Txn, Trx1 and ADF.
Claims5
A genetically modified rat whose genome comprises a mutation in an endogenous thioredoxin 1 (TXN1) gene, wherein the genetically modified rat expresses an F54L TXN1 mutant and exhibits hypertension, rupture of the tunica media of blood vessels, calcification of blood vessels, fibrosis of a heart, inflammatory cell infiltration of a heart, and myocardial dilation by three months old.
A genetically modified rat whose genome comprises a mutation in an endogenous thioredoxin 1 (TXN1) gene, wherein the genetically modified rat expresses an F54L TXN1 mutant and exhibits glomerulosclerosis, intratubular and extravascular cell hyperproliferation of the kidney, mesangial cell hyperproliferation, tubular atrophy, dilation, and necrosis of the kidney, and interstitial fibrosis of the kidney by three months old.
A genetically modified rat whose genome comprises a mutation in an endogenous thioredoxin 1 (TXN1) gene, wherein the genetically modified rat expresses an F54L TXN1 mutant and exhibits age-dependent epilepsy at least by 4- to 5-weeks-old.
Dependencies are inferred from the claim text.