癌基因刺激 KEAP1 应激信号枢纽导致 NRF2 旁路激活和 NRF2 靶基因诱导，促进肿瘤存活。
Oncogene-Stimulated Congestion at the KEAP1 Stress Signaling Hub Allows Bypass of NRF2 and Induction of NRF2-Target Genes that Promote Tumor Survival.
机构信息
Division of Cancer Research, Jacqui Wood Cancer Centre, Ninewells Hospital and Medical School, University of Dundee, Dundee DD1 9SY, Scotland.
Division of Cancer Research, Jacqui Wood Cancer Centre, Ninewells Hospital and Medical School, University of Dundee, Dundee DD1 9SY, Scotland.
出版信息
Cancer Cell. 2017 Nov 13;32(5):539-541. doi: 10.1016/j.ccell.2017.10.009.
In this issue of Cancer Cell, Ge et al. show that overexpression of the oncoprotein iASPP in cancer cells provokes NRF2-mediated induction of cytoprotective genes, because it logjams the ubiquitin ligase substrate adaptor function of KEAP1 by virtue of the fact that it possesses a novel DLT-containing KEAP1-interaction motif.
在本期《癌细胞》中，葛等研究人员表明，癌蛋白 iASPP 的过表达会促使 NRF2 介导细胞保护基因的诱导，因为它通过具有新型 DLT 包含的 KEAP1 相互作用基序，干扰 KEAP1 泛素连接酶底物衔接子的功能。
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