Roles of novel target genes of Cdx1/2 in differentiation and transformation of intestinal epithelial cells.
Project/Area Number |
20390110
|
Research Category |
Grant-in-Aid for Scientific Research (B)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Experimental pathology
|
Research Institution | Kyoto University |
Principal Investigator |
AOKI Masahiro Kyoto University, 分子病態学部, 部長 (60362464)
|
Project Period (FY) |
2008 – 2010
|
Project Status |
Completed (Fiscal Year 2010)
|
Budget Amount *help |
¥19,630,000 (Direct Cost: ¥15,100,000、Indirect Cost: ¥4,530,000)
Fiscal Year 2010: ¥6,240,000 (Direct Cost: ¥4,800,000、Indirect Cost: ¥1,440,000)
Fiscal Year 2009: ¥6,370,000 (Direct Cost: ¥4,900,000、Indirect Cost: ¥1,470,000)
Fiscal Year 2008: ¥7,020,000 (Direct Cost: ¥5,400,000、Indirect Cost: ¥1,620,000)
|
Keywords | 大腸癌 / 転写因子 / 短鎖脂肪酸 / GEF / CDX2 / PLEKHG1 / ノックアウトマウス / 14-3-3 / SLC5A8 / 酪酸 / CDX1 |
Research Abstract |
Expression of the Slc5a8 gene encoding a short-chain fatty acid transporter was positively regulated by Cdx1/2 in vivo, and its level was reduced in the colonic polyps of Apc mutant mice, accompanied by decreased expression of Cdx2. Plekhg1 was shown to be a direct target gene of Cdx1/2. Plekhg1 was involved in E-cadherin-mediated cell-cell adhesion, and bound to 14-3-3 only when phosphorylated at serine 611.
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Report
(4 results)
Research Products
(40 results)