2013 Fiscal Year Final Research Report
Physiological diversity of cytosolic T3 binding protein.: Relationship between inflammation and low T3 syndrome
Project/Area Number |
23591349
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Endocrinology
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Research Institution | Fukushima Medical University (2013) Shinshu University (2011-2012) |
Principal Investigator |
SUZUKI Satoru 福島県立医科大学, 医学部, 教授 (30222061)
|
Project Period (FY) |
2011 – 2013
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Keywords | 甲状腺ホルモン / ホルモン輸送 / 細胞質 / クリスタリン / NADPH |
Research Abstract |
1. To elucidate the mechanisms of its expression, we evaluated the promoter transactivity and insulin signaling via the AP-1 site in the promoter.The results indicated that the expression of mu-crystallin was regulated through the AP-1 site in the promoter. The signals related to AP-1 activation, such as insulin signaling may have diverse effects on mu-crystallin mRNA expression. . 2.To examine the precise regulation of T3-responsive genes in the presence of CRYM, we evaluated serial alterations of T3-responsive gene expression by changing pericellular T3 concentrations in the media.The results suggest that CRYM expression increases and sustains the T3 responsiveness of genes in cells, especially with alteration of the pericellular T3 concentration.
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