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MKK7 and ARF: New players in the DNA damage response scenery

机译:MKK7和ARF:DNA损伤反应领域的新参与者

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摘要

Sensing, integrating, and processing of stressogenic signals must be followed by accurate differential response(s) for a cell to survive and avoid malignant transformation. The DNA damage response (DDR) pathway is vital in this process, as it deals with genotoxic/oncogenic insults, having p53 as a nodal effector that performs most of the above tasks. Accumulating data reveal that other pathways are also involved in the same or similar processes, conveying also to p53. Emerging questions are if, how, and when these additional pathways communicate with the DDR axis. Two such stress response pathways, involving the MKK7 stress-activated protein kinase (SAPK) and ARF, have been shown to be interlocked with the ATM/ATR-regulated DDR axis in a highly ordered manner. This creates a new landscape in the DDR orchestrated response to genotoxic/oncogenic insults that is currently discussed.
机译:应激信号的传感,整合和处理后,必须要有精确的差分反应才能使细胞存活并避免恶性转化。 DNA损伤反应(DDR)途径在此过程中至关重要,因为它涉及遗传毒性/致癌性侵害,p53作为节点效应物,可以执行上述大多数任务。积累的数据表明,其他途径也参与相同或相似的过程,也传递给p53。新出现的问题是这些附加路径是否,如何以及何时与DDR轴通信。已显示涉及MKK7应激激活蛋白激酶(SAPK)和ARF的两种此类应激反应途径以高度有序的方式与ATM / ATR调节的DDR轴互锁。这为目前讨论的DDR对遗传毒性/致癌性侮辱的协调反应创造了新的格局。

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