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来自国际顶尖团队的研究人员针对炭疽致死毒素 (LT)引发MEKs蛋白水解失活、导致ERK/p38/JNK信号通路中断的致命机制，创新性构建了抗蛋白酶解的MEK2 (P10V/A11D)、MEK3 (I27D)和MEK6 (I15D)突变体。转基因小鼠实验证实，这些突变体可维持ERK/p38通路持续激活，显著提升宿主细胞在LT或炭疽杆菌攻击下的存活率，为毒素内化后的靶向治疗开辟新途径。

University of Pittsburgh researchers discovered that a mix of growth factors can rescue cells from late-stage anthrax damage ...

Anthrax, an infectious disease caused by the bacterium Bacillus anthracis, is often treatable in its early stages. But once ...

Surprisingly, this process does not rely on reactivating the BRAF-ERK pathway, which is the usual resistance mechanism. Using ...

Results provide proof-of-concept that ERK pathway reactivation might be an effective, biologically based therapy to prevent anthrax-induced lethality.

To fight this, doctors often use drugs called BRAF inhibitors, such as vemurafenib, which can stop the cancer’s growth—at ...