| Project/Area Number |
25670150
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
General medical chemistry
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| Research Institution | Nagahama Institute of Bio-Science and Technology |
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Principal Investigator |
REIKO Shinkura 長浜バイオ大学, バイオサイエンス学部, 教授 (50362471)
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| Research Collaborator |
YAMADA Keisuke 長浜バイオ大学, バイオサイエンス研究科
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| Project Period (FY) |
2013-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2014: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2013: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
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| Keywords | 抗体 / 遺伝子組み換え / 体細胞突然変異 / AID / DNA修復 |
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| Outline of Final Research Achievements |
Antigen stimulation induces antibody diversification through somatic hypermutation (SHM) and class switch recombination (CSR). SHM introduces point mutations at high frequency in the variable (V) region gene, whereas CSR is a region-specific recombination that replaces the heavy chain constant region (CH) gene from Cμ to other downstream CH gene, diversifying antibody effector function without changing their antigen specificity.
Activation-induced cytidine deaminase (AID) is essential for both SHM and CSR. However, it is unknown how AID regulates two genetic events, SHM and CSR. Previous studies showed that N-terminal mutant AIDs caused selective deficiency in SHM but retained CSR, suggesting the possibility that SHM activity of AID may require the SHM-specific cofactors interacting with N-terminal region of AID. In this study, we found several candidate molecules, which were co-immunoprecipitated with AID, but not G23S (a N-terminal mutant of AID), as SHM-specific cofactors.
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