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。

在一项新的自然微生物学研究中，匹兹堡大学的研究人员表明，生长因子的混合物逆转了炭疽小鼠可能致命的细胞损伤，这表明这种方法可以适用于患者。 炭疽是一种由炭疽芽孢杆菌引起的传染病，通常在早期阶段是可以治疗的。但是，一旦这种疾病在短短几天内发展到“无法挽回的地步”，患者几乎肯定会死亡。

Polycystic ovary syndrome (PCOS) represents a significant health concern for women of reproductive age, manifesting as a ...

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 ...

Anthrax, an infectious disease caused by the bacterium Bacillus anthracis, is often treatable in its early stages. But once the disease has progressed beyond the "point of no return" after just a few ...

These included MEK1 and MEK2, which control a pathway called ERK involved in cellular division and survival, and MEK3 and MEK6, which regulate the p38 pathway that's involved in stress-induced ...

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

RAMP1 protects against HIRI by inhibiting ERK and YAP phosphorylation signal transduction, highlighting its potential as a therapeutic target for HIRI and providing a new avenue for intervention.