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How selective modulation of protein degradation governs adaptive resistance to RAS inhibition governs adaptive resistance to RAS inhibition and provide a framework for developing rational combination strategies to improve the durability of RAS-targeted therapies in PDAC is defined.
This work identifies the m6A methyltransferase METTL3 as a direct substrate of the mitotic kinase CDK1 in mammalian cells and reveals a mechanism by which transcriptional elongation is coordinated with chromosome segregation fidelity.
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