| Project/Area Number |
23770212
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Molecular biology
|
|---|
| Research Institution | Tokyo Institute of Technology (2012)
National Institute of Genetics (2011) |
|---|
Principal Investigator |
KUROKAWA Yumiko 東京工業大学, 情報生命博士教育院, 特任助教 (10381633)
|
|---|
| Project Period (FY) |
2011 – 2012
|
| Project Status |
Completed (Fiscal Year 2012)
|
| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2012: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2011: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
|
|---|
| Keywords | 組換え / 相同組換え / 修復 / DNA / Rad51 / へリカーゼ / ユビキチン / ヘリカーゼ |
|---|
| Research Abstract |
In wild type cells, homologous recombination (HR) is required for repair of double-stranded DNA breaks (DSBs). If not processed properly, DSBs could cause detrimental effects in cells such as chromosome rearrangement, cell death, tumorigenesis and so on. HR, therefore, must be tightly regulated. To clarify the molecular mechanism of regulating HR, we have characterized Rad51-mediated reactions in vitro with severalfactors (activators, mediators, helicases and ubiquitin systems).
|
