DNA repair after oxidative stress: current challenges.
DNA repair after oxidative stress: current challenges.
复制标题
DOI：
10.1016/j.cotox.2017.10.009
复制
发表时间：
2018-03
影响因子：
4.6
通讯作者：
Camargo M
中科院分区：
文献类型：
--
作者：
Van Houten B;Santa-Gonzalez GA;Camargo M
Reactive oxygen and nitrogen species damage cellular macromolecules including DNA. Cells have a robust base excision repair pathway to deal with this damage in both nuclear and mitochondrial genomes. However, mitochondria lack nucleotide excision repair. Evidence suggests that chronic oxidative stress can induce protective pathways lowering genotoxicity. Understanding oxidant injury to DNA and its repair is critical for our understanding the pathophysiology of a wide range of human disorders. Model of how chronic ROS exposure provides a protective mechanism when cells are grown at intermittent low concentration (50μM) of H2O2 and during prolonged periods (seven days). H2O2 molecules diffuse into the cell mediated by the aquaporin cell membrane protein, triggering two main cell responses: i) activating redox-sensitive mediators (e. g. PI3K/AKT, ERK1, SRC), and ii) inducing DDR through ATM and ATR sensors (red). Both signaling events promote transactivation of transcription factors augmenting gene expression of DNA repair enzymes, mainly of the BER pathway (blue), NER (green) and mismatch repair (black) converging in the ROS protective phenotype.
登录
查看更多内容
影响因子：
14.9
作者：
Christmann M;Kaina B
通讯作者：
Kaina B
DNA不匹配修复和氧化DNA损伤：对癌症生物学和治疗的影响。
影响因子：
5.2
作者：
Bridge G;Rashid S;Martin SA
通讯作者：
Martin SA
影响因子：
2.1
作者：
Correia-Melo, Clara;Passos, Joao F.
通讯作者：
Passos, Joao F.
影响因子：
4.8
作者：
Henle, ES;Han, ZX;Linn, S
通讯作者：
Linn, S
影响因子：
3.7
作者：
Cesaratto L;Codarin E;Vascotto C;Leonardi A;Kelley MR;Tiribelli C;Tell G
通讯作者：
Tell G