Regulation of Keap1-Nrf2 signaling: The role of epigenetics.
Regulation of Keap1-Nrf2 signaling: The role of epigenetics.
复制标题
DOI：
10.1016/j.cotox.2016.10.008
复制
发表时间：
2016-12
影响因子：
4.6
通讯作者：
Kong AN
中科院分区：
文献类型：
--
作者：
Cheng D;Wu R;Guo Y;Kong AN
Kelch-like ECH-associated protein 1（Keap 1）-nuclear factor erythroid 2-related factor 2（NFE 2L 2/Nrf 2）信号通路是抗氧化剂对氧化和亲电应激反应的关键参与者，并且可以在许多人类疾病中发挥作用。Nrf 2的激活或抑制已经成为治疗许多疾病如癌症的方法，并且已经彻底研究了该途径的调节。最近，表观遗传学已经成为调节Keap 1-Nrf 2的另一层。表观遗传学修饰是指在不改变DNA序列的情况下对基因表达的可遗传改变，已发现各种修饰参与调节Keap 1-Nrf 2。因此，靶向Keap 1-Nrf 2上的这些表观遗传变化为调节Keap 1-Nrf 2以治疗疾病提供了潜在的途径。在这篇综述中，几个重要的和最近的研究结果表观遗传调控和Keap 1-Nrf 2的观点进行了讨论和分享。
Kelch-like ECH-associated protein 1 (Keap1)-nuclear factor erythroid 2-related factor 2 (NFE2L2/Nrf2) signaling pathway is a pivotal player in the antioxidant response to oxidative and electrophilic stress and can play a role in many human diseases. Activation or inhibition of Nrf2 has been an approach to treating many diseases such as cancer and regulation of this pathway has been thoroughly studied. Recently, epigenetics has emerged as another layer for regulating Keap1-Nrf2. Epigenetics modification is defined as heritable changes to gene expression without changing DNA sequence and various modifications have been found to be involved in regulating Keap1-Nrf2. Therefore, targeting these epigenetic changes on Keap1-Nrf2 provides a potential pathway for modulating Keap1-Nrf2 to treat disease. In this review, several important and recent findings on epigenetic regulation and perspectives on Keap1-Nrf2 are discussed and shared.
登录
查看更多内容
影响因子：
7.7
作者：
Cheng X;Chapple SJ;Patel B;Puszyk W;Sugden D;Yin X;Mayr M;Siow RC;Mann GE
通讯作者：
Mann GE
影响因子：
9
作者：
通讯作者：
--
影响因子：
4.7
作者：
Singh, Bhupendra;Ronghe, Amruta M.;Bhat, Hari K.
通讯作者：
Bhat, Hari K.
影响因子：
11.5
作者：
Chase, Andrew;Cross, Nicholas C. P.
通讯作者：
Cross, Nicholas C. P.
DOI：
10.1158/1940-6207.capr-14-0127
发表时间：
2014-12
期刊：
Cancer prevention research (Philadelphia, Pa.)
影响因子：
--
作者：
Khor TO;Fuentes F;Shu L;Paredes-Gonzalez X;Yang AY;Liu Y;Smiraglia DJ;Yegnasubramanian S;Nelson WG;Kong AN
通讯作者：
Kong AN