DCLK1与DNA损伤反应

J. Panneerselvam, D. Qu, C. Houchen, M. Bronze, P. Chandrakesan
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引用次数: 0

摘要

基因组完整性由复杂的细胞网络不断监测,统称为DNA损伤反应(DDR)。DDR是一个信号网络,包括细胞周期检查点和DNA修复和损伤耐受途径。DDR的失败或相关事件会导致各种疾病,包括癌症。DDR主要由磷脂酰肌醇-3激酶样蛋白激酶(PIKKs)家族成员共济失调毛细血管扩张突变(ATM)和共济失调毛细血管扩张及rad3相关蛋白(ATR)介导。然而,关于这些信号转导途径的许多悬而未决的问题之一是:细胞是如何打开DDR信号的?在我们最近研究DCLK1在基因毒性损伤后调控ATM中的作用之前,没有确凿的证据表明特定的感觉激酶参与DDR信号。目前,各种研究都在证明DCLK1在DNA损伤反应中的重要性。在这里,我们讨论了DCLK1在DNA损伤反应中的作用的新见解。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
DCLK1 and DNA Damage Response
Genome integrity is constantly monitored by sophisticated cellular networks, collectively termed as the DNA damage response (DDR). The DDR is a signaling network that includes cell cycle checkpoints and DNA repair and damage tolerance pathways. Failure of the DDR or associated events causes various diseases, including cancer. DDR is primarily mediated by phosphatidylinositol-3-kinase-like protein kinase (PIKKs) family members ataxia-telangiectasia mutated (ATM) and ataxia telangiectasia and Rad3-related protein (ATR). However, one of the many unanswered questions regarding these signal-transduction pathways is: how does the cell turn the DDR signals on? There was no conclusive demonstration of the involvement of a specific sensory kinase in DDR signals until our recent research on the DCLK1 role in regulating ATM after genotoxic injury. Currently, various studies are demonstrating the importance of DCLK1 in DNA damage response. Here, we discuss the novel insights into the role of DCLK1 in DNA damage response.
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