title: Epigenomic Regulation of Smad1 Signaling During Cellular Senescence Induced by Ras Activation.
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.
authors.affiliation: 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. kaneda@genome.rcast.u-tokyo.ac.jp.|Department of Molecular Oncology, Graduate School of Medicine, Chiba University, Chiba, Japan. kaneda@genome.rcast.u-tokyo.ac.jp.|CREST, Japan Science and Technology Agency, Saitama, Japan. kaneda@genome.rcast.u-tokyo.ac.jp.
authors.forename: Atsushi
authors.initials: A
authors.lastname: Kaneda
authors.affiliation: 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.
authors.forename: Aya
authors.initials: A
authors.lastname: Nonaka
authors.affiliation: 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.
authors.forename: Takanori
authors.initials: T
authors.lastname: Fujita
authors.affiliation: 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.
authors.forename: Ryota
authors.initials: R
authors.lastname: Yamanaka
authors.affiliation: 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.
authors.forename: Mai
authors.initials: M
authors.lastname: Fujimoto
authors.affiliation: Department of Molecular Pathology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
authors.forename: Kohei
authors.initials: K
authors.lastname: Miyazono
authors.affiliation: 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.
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Aburatani
mesh_terms: D000818:Animals; D002461:Cell Line, Transformed; D016922:Cellular Senescence / Q000502:physiology*; D047369:Chromatin Immunoprecipitation; D044127:Epigenesis, Genetic; D057890:Epigenomics / Q000379:methods; D005347:Fibroblasts; D015870:Gene Expression; D005786:Gene Expression Regulation; D017930:Genes, Reporter; D059014:High-Throughput Nucleotide Sequencing; D006657:Histones / Q000378:metabolism; D051379:Mice; D060888:Real-Time Polymerase Chain Reaction; D015398:Signal Transduction; D051898:Smad1 Protein / Q000378:metabolism*; D015533:Transcriptional Activation; D018631:ras Proteins / Q000235:genetics*
chemical_list: D006657:Histones; D051898:Smad1 Protein; D018631:ras Proteins
keywords: Bmp2; Chromatin immunoprecipitation (ChIP); Epigenetics; Histone; Smad1