How Does MTAP Deletion Create a Therapeutic Window for PRMT5 Inhibition? — Mechanistic Basis from MTA Accumulation to MTA-Cooperative PRMT5 Inhibitors
In 2016, two independent studies published in Science found that cancer cells deficient in methylthioadenosine phosphorylase (MTAP) were more sensitive to partial depletion of protein arginine methyltransferase 5 (PRMT5).[1,2] This finding emerged from large-scale functional genomic screens and ...
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