| Co-Investigator(Renkei-kenkyūsha) |
SHINKURA Reiko 長浜バイオ大学, バイオサイエンス部, 教授 (50362471)
BEGUM Nasim 京都大学, 医学研究科, 准教授 (80362507)
NAGAOKA Hitoshi 岐阜大学, 医学研究科, 教授 (20270647)
CHON Il-Mi 徳島大学, 疾患ゲノム研究センター, 助教 (50452339)
KOBAYASHI Maki 京都大学, 医学研究科, 准教授 (20400690)
DOI Tomomitsu 慶應大学, 医学研究科, 助教 (70437218)
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| Budget Amount *help |
¥764,400,000 (Direct Cost: ¥588,000,000、Indirect Cost: ¥176,400,000)
Fiscal Year 2009: ¥136,370,000 (Direct Cost: ¥104,900,000、Indirect Cost: ¥31,470,000)
Fiscal Year 2008: ¥136,370,000 (Direct Cost: ¥104,900,000、Indirect Cost: ¥31,470,000)
Fiscal Year 2007: ¥190,190,000 (Direct Cost: ¥146,300,000、Indirect Cost: ¥43,890,000)
Fiscal Year 2006: ¥147,160,000 (Direct Cost: ¥113,200,000、Indirect Cost: ¥33,960,000)
Fiscal Year 2005: ¥154,310,000 (Direct Cost: ¥118,700,000、Indirect Cost: ¥35,610,000)
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| Research Abstract |
We found that AID down-modulates translation of topoisomerase (Top1). The reduction of Top1 induces aberrant DNA structure in transcribed S regions, resulting in irreversible cleavage by Top1. We propose that AID edits microRNA and edited microRNA down-modulates translation of Top1 mRNA. AID was shown to be expressed not only in lymphoma but also pathogen-induced tumors. We investigated the AID promoter and identified positive and negative regulatory elements, which may explain such AID induction. We examined DNA deamination hypothesis and obtained the following evidence against this hypothesis. 1) AID mutant without DNA deamination activity is proficient for CSR. 2) UNG mutants of the protein interaction domain with normal U removal activity lost CSR activity. 3) APE1 and APE2 deficiency did not reduce CSR.
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