Identification of Smad cofactors involved in tumor progression
| Project/Area Number |
16H05150
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (B)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Pathological medical chemistry
|
|---|
| Research Institution | University of Yamanashi |
|---|
Principal Investigator |
MIYAZAWA KEIJI 山梨大学, 大学院総合研究部, 教授 (40209896)
|
|---|
| Research Collaborator |
ITOH yuka
MOTIZUKI mitsuyoshi
MIYAKE kunio
|
|---|
| Project Period (FY) |
2016-04-01 – 2019-03-31
|
| Project Status |
Completed (Fiscal Year 2018)
|
| Budget Amount *help |
¥17,550,000 (Direct Cost: ¥13,500,000、Indirect Cost: ¥4,050,000)
Fiscal Year 2018: ¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2017: ¥5,980,000 (Direct Cost: ¥4,600,000、Indirect Cost: ¥1,380,000)
Fiscal Year 2016: ¥6,240,000 (Direct Cost: ¥4,800,000、Indirect Cost: ¥1,440,000)
|
|---|
| Keywords | シグナル伝達 / TGF-β / Smad / 転写活性化 / がん / 癌 |
|---|
| Outline of Final Research Achievements |
In the present study, we worked on Smad cofactors in cancer cells, which enable a wide variety of cell responses induced by TGF-β. We identified Olig1 as a Smad cofactor involved in anti-apoptotic function of TGF-β in murine breast cancer cells. We also developed a strategy to screen Smad cofactors that operate in cancer cells and identified two novel Smad cofactors. Furthermore, we found minimal requirements for transcription activation by cooperation of Smad and Smad cofactors.
|
| Academic Significance and Societal Importance of the Research Achievements |
TGF-βの多様な作用の一部のみを選択的に抑制する次世代のTGF-β阻害薬開発のためには、個々の作用に密接に結びついたSmad cofactorを同定し、その機能の発現メカニズムを明らかにする必要がある。本研究では新規Smad cofactorの探索法を開発するとともに、Smad cofactorの作用を効率的にブロックする手法を開発するための基礎として、SmadとSmad cofactorによる協調的な転写活性化の必要条件を明らかにした。
|
Report
(4 results)
Research Products
(11 results)
