1995 Fiscal Year Final Research Report Summary
A Study of Transgenic Mouse Carrying the Mutant cDNA of Thyroid Hormone Receptor Beta
| Project/Area Number |
05670683
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Pediatrics
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| Research Institution | KAGOSHIMA UNIVERSITY |
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Principal Investigator |
TAKEI Shuji Kagoshima Univ., Faculty of Medicine, Assitant Professor, 医学部, 講師 (60175437)
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| Co-Investigator(Kenkyū-buntansha) |
OKU Syozo Kagoshima Univ., Faculty of Medicine, Research Associate, 医学部, 助手 (80224145)
IMANAKA Hiroyuki Kagoshima Univ., Faculty of Medicine, Research Associate, 医学部, 助手 (80223329)
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| Project Period (FY) |
1993 – 1995
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| Keywords | Transgenic mouse / Thyroid hormone receptor beta / Animal model / Dominant negative effect / Thyroid hormone resistance syndrome |
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| Research Abstract |
The syndrome of thyroid hormone resistance was firstly described by Refetoff et al., and more than 350 reports were published about this disease. Many of investigations are also published for understanding of physiology of the disease and of thyroid hormone effect in vivo. There is variability in the degree of resistance in different target tissues within an individual and clinical phenotype varies in different patients. There are many reports about the interaction of the thyroid hormone and its receptor in vivo. However, mechanism of clinical phenotype varies in this disease have not been completely understood.
In order to know the interaction of thyroid hormone and its receptor in vivo, and to know the physiological mechanisms of the human thyroid hormone resistance disease, we produced the transgenic mice carrying the mutant cDNA of thyroid hormone receptor beta. The mutant cDNA was isolated from a patient with thyroid hormone-resistance syndrome. We infected the mutant cDNA into mouse fertilized eggs and produced 6 transgenic mice. Four lines of transgenic mouse were established. All mouse lines were expressed the mutant gene. There were various phenotypes in these transgenic mice ; i.e., growth retardation, decreased spontaneous behavior and baldness. These phenotypic variations are also observed in human thyroid hormone resistance syndrome.
We concluded that these transgenic mice were animal model for the resistance syndrome. These mice would be useful for investigation of the thyroid hormone-resistance mechanism.
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Research Products
(10 results)
