Kotsinas Athanassios, Papanagnou Panagiota, Galanos Panagiotis, Schramek Daniel, Townsend Paul, Penninger Josef M, Bartek Jiri, Gorgoulis Vassilis G
Molecular Carcinogenesis Group; Department of Histology and Embryology; School of Medicine; University of Athens; Athens, Greece.
Howard Hughes Medical Institute; Laboratory of Mammalian Cell Biology and Development; The Rockefeller University; New York, NY USA.
Cell Cycle. 2014;13(8):1227-36. doi: 10.4161/cc.28654. Epub 2014 Mar 26.
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.
应激信号的感知、整合和处理之后,细胞必须做出准确的差异反应才能存活并避免恶性转化。DNA损伤反应(DDR)通路在这一过程中至关重要,因为它应对基因毒性/致癌性损伤,p53作为关键效应因子执行上述大部分任务。越来越多的数据表明,其他通路也参与相同或类似的过程,并且也与p53相关。新出现的问题是这些额外的通路是否、如何以及何时与DDR轴进行沟通。两条这样的应激反应通路,涉及MKK7应激激活蛋白激酶(SAPK)和ARF,已被证明以高度有序的方式与ATM/ATR调节的DDR轴相互关联。这为当前所讨论的DDR精心编排的对基因毒性/致癌性损伤的反应创造了新的局面。