Ras激活诱导细胞衰老过程中Smad1信号通路的表观基因组调控

Epigenomic Regulation of Smad1 Signaling During Cellular Senescence Induced by Ras Activation.

作者信息

Kaneda Atsushi, Nonaka Aya, Fujita Takanori, Yamanaka Ryota, Fujimoto Mai, Miyazono Kohei, Aburatani Hiroyuki

机构信息

Genome Science Division, Research Center for Advanced Science and Technology (RCAST), The University of Tokyo, 4-6-1 Komaba, Meguro-ku, Tokyo, 153-8904, Japan.

Department of Molecular Oncology, Graduate School of Medicine, Chiba University, Chiba, Japan.

出版信息

Methods Mol Biol. 2016;1344:341-53. doi: 10.1007/978-1-4939-2966-5_22.

DOI:10.1007/978-1-4939-2966-5_22

PMID:26520136

Abstract

Epigenomic modification plays important roles in regulating gene expression during development, differentiation, and cellular senescence. When oncogenes are activated, cells fall into stable growth arrest to block cellular proliferation, which is called oncogene-induced senescence. We recently identified through genome-wide analyses that Bmp2-Smad1 signal and its regulation by harmonized epigenomic alteration play an important role in Ras-induced senescence of mouse embryonic fibroblasts. We describe in this chapter the methods for analyses of epigenomic alteration and Smad1 targets on genome-wide scale.

摘要

表观基因组修饰在发育、分化和细胞衰老过程中调节基因表达方面发挥着重要作用。当癌基因被激活时，细胞会陷入稳定的生长停滞以阻止细胞增殖，这被称为癌基因诱导的衰老。我们最近通过全基因组分析发现，Bmp2-Smad1信号及其通过协调的表观基因组改变的调控在Ras诱导的小鼠胚胎成纤维细胞衰老中起重要作用。在本章中，我们描述了在全基因组范围内分析表观基因组改变和Smad1靶点的方法。