Project/Area Number |
22591495
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Digestive surgery
|
Research Institution | Toho University |
Principal Investigator |
|
Co-Investigator(Renkei-kenkyūsha) |
KANNO Shin-ichiro 東北大学, 加齢医学研究所, 講師 (10400417)
|
Project Period (FY) |
2010 – 2012
|
Project Status |
Completed (Fiscal Year 2012)
|
Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2012: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2011: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2010: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
|
Keywords | 小腸大腸肛門外科学 / 低酸素 / 腫瘍微小環境 / 転写制御 / MLH1 / CXXC5 / DNAミスマッチ修復遺伝子 / 低酸素状態 / SYF2 / hnRPH1 / 転写制御因子 |
Research Abstract |
In this study, CXXC5, DNA-binding protein recognizing the FP3CAT site of MLH1 promoter, was identified as an activator of MLH1 transcription. Co-immunoprecipitation and LC/MS/MS analysis revealed that CXXC5 and SYF2, previously screened as an FP3 site-binding protein, share common interacting protein HNRNPH1 and may co-operatively trans-activate MLH1. In hypoxia, all three protein levels were down-regulated and endogenous over-expression of them partially rescued MLH1 down-regulation. Hypoxic down-regulationof MLH1 may be mediated by CXXC5, SYF2, and HNRNPH1.
|