Identifying ubiquitous genomic enhancer elements required for epithelial differentiation
| Project/Area Number |
17K17978
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Experimental pathology
General anatomy (including histology/embryology)
|
|---|
| Research Institution | Fukushima Medical University |
|---|
Principal Investigator |
|
|---|
| Project Period (FY) |
2017-04-01 – 2019-03-31
|
| Project Status |
Completed (Fiscal Year 2018)
|
| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2018: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2017: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
|
|---|
| Keywords | 核内受容体 / 細胞接着 / シグナル伝達 / 細胞分化 / エンハンサー / 上皮分化 / レチノイン酸 / タイト結合 / ゲノム編集 |
|---|
| Outline of Final Research Achievements |
The basis of cell adhesion signaling is poorly understood. We identify a link between tight-junction molecule claudin-6 and retinoic acid receptor signaling to initiate epithelial differentiation. This signaling axis resulted in phosphorylation of RAR gamma; at S379, which was conserved across species and was indispensable for both releasing the nuclear receptor corepressor (NCoR) from retinoic acid (RA) response elements in target genes, thereby driving epithelialization. This novel crosstalk provides a new insight into the transcription regulation by cell adhesion.
|
| Academic Significance and Societal Importance of the Research Achievements |
細胞の遺伝子発現を制御するシグナルの起点は細胞外のタンパク質や小分子がレセプターに結合することを起点とすると考えられてきた。ところが我々は細胞間接着に端を発するシグナルが、転写因子の1つである核内受容体のリン酸化を引き起こし、リガンドに対する感受性を高めることでその標的遺伝子の発現に影響することを突き止めた。この新規シグナル経路は種や細胞種を超えて様々な分子で広く保存されている可能性があり、これに着目した生命現象や病態解明が期待される。
|
Report
(3 results)
Research Products
(13 results)
