Project/Area Number |
20510048
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Risk sciences of radiation/Chemicals
|
Research Institution | Chiba University |
Principal Investigator |
SUZUKI Nobuo Chiba University, 大学院・医学研究院, 教授 (90111426)
|
Co-Investigator(Kenkyū-buntansha) |
KITA Kazuko 千葉大学, 大学院・医学研究院, 講師 (80302545)
SUGAYA Shigeru 千葉大学, 大学院・医学研究院, 助教 (90334177)
SUZUKI Toshikazu 千葉大学, 大学院・医学研究院, 助教 (70270527)
|
Project Period (FY) |
2008 – 2010
|
Project Status |
Completed (Fiscal Year 2010)
|
Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2010: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2009: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2008: ¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
|
Keywords | ヒト / 放射線 / 変異 / シャペロン / プロテアーゼ / 血清 / 細胞 / DNA修復 / ヒト細胞 / マイクロRNA |
Research Abstract |
The following two points were mainly identified in mechanisms which regulate mutability in human. (1) When the HSP27 and annexin II complex is involved in DNA repair pathways for UVC-caused DNA damages, HSP27 may protect annexin II from the breakdown after UVC irradiation. Annexin II is released from cells and the released one may be involved in cellular UVC-resistance via signal transduction pathways. (2) The miRNAs, which may be involved in cell growth and mutation, were found.
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