Epigenetically Silencing(表观遗传沉默)研究综述
Epigenetically Silencing 表观遗传沉默 - Epigenetically silencing of Hif1α via histone H3 methylation in the promoter region was achieved by CRISPR/dCas9-EZH2 system, in which histone H3 methylase EZH2 was recruited to the promoter region specifically. [1] EZH2 is a core component of the polycomb repressive complex 2 (PRC2), which catalyzes trimethylation of histone H3 lysine 27 (H3K27me3) and promotes carcinogenesis by epigenetically silencing many tumor suppressor genes. [2]通过 CRISPR/dCas9-EZH2 系统通过启动子区域中的组蛋白 H3 甲基化实现 Hif1α 的表观遗传沉默,其中组蛋白 H3 甲基化酶 EZH2 被特异性募集到启动子区域。 [1] EZH2 是多梳抑制复合物 2 (PRC2) 的核心成分,可催化组蛋白 H3 赖氨酸 27 (H3K27me3) 的三甲基化,并通过表观遗传沉默许多肿瘤抑制基因来促进致癌作用。 [2]
β catenin signaling
Collectively, we determined that STAT1-induced upregulation of LINC00467 promoted LUAD progression by epigenetically silencing DKK1 to activate Wnt/β-catenin signaling pathway. [1] It was uncovered that FOXD2-AS1 enhanced the activity of Wnt/β-catenin signaling pathway by epigenetically silencing the inhibitor of Wnt/β-catenin signaling pathway (DKK1). [2]总的来说,我们确定 STAT1 诱导的 LINC00467 上调通过表观遗传沉默 DKK1 以激活 Wnt/β-catenin 信号通路来促进 LUAD 进展。 [1] 发现FOXD2-AS1通过表观遗传沉默Wnt/β-catenin信号通路抑制剂(DKK1)来增强Wnt/β-catenin信号通路的活性。 [2]