期刊
CELL CYCLE
卷 13, 期 8, 页码 1227-1236出版社
TAYLOR & FRANCIS INC
DOI: 10.4161/cc.28654
关键词
p53; feedback loop; ARF; anti-tumor barrier; MKK7; senescence; Wip-1; p38 MAPK; replication stress; DNA damage response
类别
资金
- European Commission [284460, CZ.1.05/2.1.00/01.0030]
- Era of Hope/Department of Defense
- Advanced ERC grant
- Empeirikeion Foundation fellowship
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.
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