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PRMT9-mediated arginine methylation drives venetoclax resistance in AML by altering RNA splicing and protein synthesis. Targeting PRMT9 restores venetoclax sensitivity, offering a promising approach to combat resistant AML.
This review explores how PRMT9-mediated symmetric dimethylation of STAT1 serves as a critical check on proinflammatory macrophage activation, offering a novel therapeutic target for mitigating cardiac injury following myocardial infarction.
Researchers have discovered that the protein PRMT9 plays a vital role in healing the heart after a myocardial infarction by controlling inflammatory macrophages. By promoting the degradation of the STAT1 protein, PRMT9 reduces tissue damage