Kyoto University · 生化学・遺伝学・分子生物学
Takeda教授の研究室では、哺乳類細胞におけるDNA修復機構、特に塩基除去修復（BER）の分子メカニズムを解明しています。特に、XRCC1というシルクレースタンプタンパク質がPARP1の過剰な活性化を制御し、修復過程でのタンパク質の「トラップ」を防ぐ役割を明らかにしています。この研究は、がん治療におけるPARP阻害剤の効果メカニズムや遺伝性疾患の病態解明にも寄与しています。
Figures are computed from collected data and may differ slightly.
Mammalian DNA base excision repair (BER) is accelerated by poly(ADP-ribose) polymerases (PARPs) and the scaffold protein XRCC1. PARPs are sensors that detect single-strand break intermediates, but the critical role of XRCC1 during BER is unknown. Here, we show that protein complexes containing DNA polymerase β and DNA ligase III that are assembled by XRCC1 prevent excessive engagement and activity of PARP1 during BER. As a result, PARP1 becomes "trapped" on BER intermediates in XRCC1-deficient c
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