Molecular mechanism of E2F regulation of cell proliferation and tumor suppression
| Project/Area Number |
15K06957
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Multi-year Fund |
|---|
| Section | 一般 |
|---|
| Research Field |
Molecular biology
|
|---|
| Research Institution | Kwansei Gakuin University |
|---|
Principal Investigator |
|
|---|
| Project Period (FY) |
2015-04-01 – 2018-03-31
|
| Project Status |
Completed (Fiscal Year 2017)
|
| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2017: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
|
|---|
| Keywords | E2F / RB / ARF / p53 / がん化抑制 / 細胞増殖 / がん抑制遺伝子 / pRB / リン酸化 / 相互作用因子 / CDK |
|---|
| Outline of Final Research Achievements |
We examined the molecular mechanism of how the transcription factor E2F, the principal target of the tumor suppressor RB, discriminates between growth-related genes and tumor suppressor genes. We examined the possibility of differential phosphorylation of E2F1, which plays major roles in tumor suppression, by generating mutants of 65 sites that could be phosphorylated. No mutants showed differential ability to activate tumor suppressor genes. We thought of the possibility that different cofactors contribute to activation of growth-related genes and tumor suppressor genes. We explored novel factors, which interacts with E2F1 by co-immunoprecipitation and yeast two-hybrid system. These screening gave 3 and 20 candidates, respectively. We analyzed these factors and found that DDX5, WDR1 and GTF2H2 enhance E2F1 activation of tumor suppressor genes.
|
Report
(4 results)
Research Products
(19 results)
