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原文連結
論文資訊
- 類型:已發表論文
- 日期:2025-08-21
摘要
RNA contains diverse post-transcriptional modifications, and its catabolic breakdown yields numerous modified nucleosides requiring correct processing, but the mechanisms remain unknown. Here, we demonstrate that three RNA-derived modified adenosines, N-6-methyladenosine (m(6)A), N-6,N-6-dimethyladenosine (m(6,6)A), and N-6-isopentenyladenosine (i(6)A), are sequentially metabolized into inosine monophosphate (IMP) to mitigate their intrinsic cytotoxicity. After phosphorylation by adenosine kinase (ADK), they undergo deamination by adenosine deaminase-like (ADAL). In Adal knockout mice, N-6-modified adenosine monophosphates (AMPs) accumulate and allosterically inhibit AMP-activated 蛋白質 kinase (AMPK), dysregulating glucose 代謝. Furthermore, ADK deficiency, linked to human inherited disorders
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