Cyp26b1 regulates the expression of the gut-homing receptor CCR9 in T cells.
Project/Area Number |
19590264
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
General pharmacology
|
Research Institution | Tokushima Bunri University |
Principal Investigator |
TAKEUCHI Hajime Tokushima Bunri University, 香川薬学部, 助教 (00421298)
|
Project Period (FY) |
2007 – 2009
|
Project Status |
Completed (Fiscal Year 2009)
|
Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2009: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2008: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2007: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
|
Keywords | 炎症・免疫 / レチノイン酸 / 生体分子 / 発現制御 / 免疫学 / ホーミング |
Research Abstract |
All-trans retinoic acid (AtRA) is an essential regulator in lymphocyte. Concentrations of AtRA are maintained by the balance between synthesis and degradation. CYP26 metabolizes AtRA into inactive derivatives. We found that Cyp26b1, one of CYP26 enzymes, was expressed in T cells in gut-related lymphoid organs. The expression level of Cyp26b1 was significantly related to the AtRA-induced expression of the gut-homing receptor.
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Report
(4 results)
Research Products
(13 results)