| Project/Area Number |
22570137
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Functional biochemistry
|
|---|
| Research Institution | Tokyo Institute of Technology |
|---|
Principal Investigator |
TANAKA Toshiaki 東京工業大学, 大学院・生命理工学研究科, 助教 (40263446)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
TAKAHASHI Shuji 東京大学, 教養学部, 特任准教授 (90447318)
|
|---|
| Project Period (FY) |
2010 – 2012
|
| Project Status |
Completed (Fiscal Year 2012)
|
| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2011: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2010: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
|
|---|
| Keywords | ホルモンと生理活性物質 / 肝細胞増殖因子 / 癌 / ID1 / 不可逆的増殖停止 / Skp2 / Myc / 遺伝子発現 / エピジェネティクス / シグナル伝達 / 除放剤 / 転写制御 / プロモーターアッセイ / HepG2 |
|---|
| Research Abstract |
HGF treatment of HepG2 hepatoma cells decreases expression of an oncogene ID1. This study showed that the decrease in ID1 is regulated through downregulation of Skp2, a component of E3 ubiquitin ligase, in the presence of HGF. However, Skp2 was involved in the regulation of ID1 expression by regulating transcription activity of Myc independently of ubiquitination. This study also showed that G9a histone methyltransferase, which expression may be regulated through Skp2/Myc/ID1, is involved in the alteration of H3K9me3 localization in cell nuclei induced by HGF, leading to the irreversible suppression of cancer cell proliferation by HGF.
|
