| Project/Area Number |
13470522
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Laboratory medicine
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| Research Institution | Dokkyo University School of Medicine |
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Principal Investigator |
IEIRI Tamio Dokkyo University School of Medicine, Professor, 医学部, 教授 (80049220)
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| Co-Investigator(Kenkyū-buntansha) |
HISHINUMA Akira Dokkyo University School of Medicine, Associate Professor, 医学部, 助教授 (40201727)
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| Project Period (FY) |
2001 – 2003
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| Project Status |
Completed (Fiscal Year 2003)
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| Budget Amount *help |
¥14,000,000 (Direct Cost: ¥14,000,000)
Fiscal Year 2003: ¥4,200,000 (Direct Cost: ¥4,200,000)
Fiscal Year 2002: ¥4,900,000 (Direct Cost: ¥4,900,000)
Fiscal Year 2001: ¥4,900,000 (Direct Cost: ¥4,900,000)
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| Keywords | Cretinism / thyroid dysgenesis / thyroid transcription factor-2 / thyroid / quantitative reverse transcription-polymerase chain reaction / tissue specificity / T1560 gene / T1560遺伝子 / 甲状腺形成異状 / 甲状腺原基 / TTF-2転写因子 / cDNAアレイ / マイクロアレイ / 定量的PCR法 / サブトラクションPCR法 / 遺伝発現 / アラニン反復回数 |
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| Research Abstract |
Thyroid dysgenesis is the most frequent cause of congenital hypothyroidism, but its molecular pathophysiology is largely unknown. Our hypothesis that. some genes downstream to thyroid transcription factor-2 (TTF-2) might be responsible for development of the thyroid prompted us to identify genes whose expression is stimulated by TTF-2. PCR product of cDNA clones obtained by a subtraction PCR method in TTF-2 expressing cell lines were screened with labeled cDNA by microarray analysis. We isolated 17 genes up-regulated by TTF-2, which were subsequently confirmed by quantitative RT-PCR. One of them is a novel gene designated T1560 that showed a highly thyroid-spesific expression pattern. Luciferase reporter assays showed that expression of all of the 14 genes tested was stimulated by both TTF-2 and TTF-1, another thyroid specific transcription factor. Our results have important implications for understanding normal thyroid development as well as the molecular defects underlying thyroid dysgenesis.
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