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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.
This study establishes a comprehensive multi-omics resource for KRAS signalling in PDAC and demonstrates that cellular context exerts a stronger influence than allele identity in shaping molecular profiles, with implications for interpreting putative allele-specific signalling dependencies.
A multi-omics framework that infers context-specific protein activities from transcriptomic, phosphoproteomic, and protein correlation-based protein-protein interaction data is introduced, integrating modality-specific algorithms via network diffusion.
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