RBM15B recognizes H3K79me2 to guide selective mA-modification of mRNA and enhance oncoprotein translation in MLL-r leukemia.
1/5 보강
The distribution of N-methyladenosine (mA) controls its substrate RNA fate, playing key roles in various biological processes.
APA
Chen TQ, Sun YM, et al. (2026). RBM15B recognizes H3K79me2 to guide selective mA-modification of mRNA and enhance oncoprotein translation in MLL-r leukemia.. The EMBO journal, 45(5), 1672-1696. https://doi.org/10.1038/s44318-026-00707-1
MLA
Chen TQ, et al.. "RBM15B recognizes H3K79me2 to guide selective mA-modification of mRNA and enhance oncoprotein translation in MLL-r leukemia.." The EMBO journal, vol. 45, no. 5, 2026, pp. 1672-1696.
PMID
41629530 ↗
Abstract 한글 요약
The distribution of N-methyladenosine (mA) controls its substrate RNA fate, playing key roles in various biological processes. However, the mechanism underlying site-selective mA deposition of RNAs, especially in the start codon regions, and the role in epigenetic information transduction connecting tumorigenesis remain largely unknown. Here, we identified RBM15B mainly modulates mA modifications in the 5'untranslated regions (UTRs) and around the start codons of mRNAs transcribed. This process is guided by H3K79me2 histone methylation, a critical epigenetic modification in mixed lineage leukemia. We show that the H47 of RBM15B is a key residue for the recognition of H3K79me2. The selective mA modification orchestrated by the H3K79me2-RBM15B axis enhances translation efficiency of oncogenic transcripts, and promotes self-renewal of leukemic stem cells and leukemia maintenance. We further demonstrate that blockade of the H3K79me2-RBM15B-mA axis inhibits the survival of leukemia cells and promotes cell differentiation, and impairs hematological malignancies. This study uncovers a novel selective mA deposition mechanism mediated by H3K79me2 and RBM15B, highlighting promising therapeutic targets for hematological malignancies.
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