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MTAP loss disrupts the methionine salvage pathway, resulting in the accumulation of 5′-methylthioadenosine (MTA) and partial inhibition of PRMT5 activity. Cancer cells consequently enter a state with limited PRMT5 functional reserve and develop greater dependence on residual PRMT5 activity and ...
MTAP缺失可阻断甲硫氨酸补救代谢，使5′-甲硫腺苷（MTA）积累并部分抑制PRMT5活性。癌细胞由此进入PRMT5功能余量降低的状态，对剩余PRMT5活性及SAM供应形成更强依赖，使MTAP缺失成为可利用的肿瘤代谢脆弱性。
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 ...
2016 年，两项独立发表于 Science 的研究发现，甲硫腺苷磷酸化酶（methylthioadenosine phosphorylase，MTAP）缺失的癌细胞，对蛋白精氨酸甲基转移酶5（protein arginine methyltransferase 5，PRMT5）的部分降低表现出更高敏感性[1,2]。这一发现由大规模功能基因组筛选获得，并通过 MTAP ...
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