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RIKEN IMS Annual Report 2019 RIKEN IMS Annual Report 2019
RIKEN IMS Annual Report 2019 RIKEN IMS Annual Report 2019 RIKEN Center for Integrative Medical Sciences RIKEN Center for Integrative Medical Sciences RIKEN Center for Integrative Medical Sciences Organization Chart Director Division of Genomic Medicine Tadashi Yamamoto Laboratory for Transcriptome Technology: Piero Carninci Nucleic Acid Diagnostic System Development Unit: Kengo Usui Laboratory for Cellular Function Conversion Technology: Harukazu Suzuki Preventive Medicine and Applied Genomics Unit: Hideya Kawaji Laboratory for Genome Information Analysis: Chung Chau Hon RIKEN-IFOM Joint Laboratory for Cancer Genomics: Yasuhiro Murakawa Deputy Directors Office of the Center Director Laboratory for Applied Computational Genomics: Michel De Hoon Laboratory for Genotyping Development: Yukihide Momozawa Piero Carninci Chikashi Terao Piero Carninci Laboratory for Single Cell Technologies: Laboratory for Statistical and Translational Genetics: Takeya Kasukawa Taisei Mushiroda Haruhiko Koseki Laboratory for Large-Scale Biomedical Data Technology: Laboratory for Pharmacogenomics: Jay W. Shin Taisei Mushiroda Kazuhiko Yamamoto Laboratory for Advanced Genomics Circuit: Laboratory for International Alliance on Genomic Research: Genetic Diagnosis Technology Unit: Kengo Usui Laboratory for Bone and Joint Diseases: Shiro Ikegawa Epigenome Technology Exploration Unit: Aki Minoda Laboratory for Genomics of Diabetes and Metabolism: Momoko Horikoshi Senior Advisor Laboratory for Comprehensive Genomic Analysis: Yasushi Okazaki Laboratory for Cardiovascular -
1 International Symposium on Carcinogenic Spiral & 9
1st International Symposium on Carcinogenic Spiral & 9th International Conference on Protein Phosphatase February 1 (Tue) – 3 (Thu), 2011 Tetsumon Memorial Hall, The University of Tokyo, Japan Organizer Masanori HATAKEYAMA, M.D. Ph.D. 1 Welcoming Address Welcome to the Joint Meeting of the 1st International Symposium on Carcinogenic Spiral and the 9th International Conference on Protein Phosphatase. As the organizer, I am delighted to host many eminent scholars from Japan as well as overseas. During the Conference, you will be able to learn about exciting up-to-date discoveries in the field of protein phosphatase research. I also would like to emphasize that the second day of the conference will provide a unique scientific opportunity that admixes cutting-edge research on tyrosine phosphatases with cutting-edge research on infection, inflammation and cancer. This special session was made possible by the generous support from Scientific Research on Innovative Areas, a MEXT Grant-in Aid Project. I hope that all of the participants will benefit from valuable scientific information and fruitful discussions throughout the 3-day Conference. I would like to again express a warm-hearted welcome to all of you gathered here. I also express my special thanks to those who have taken time out of their busy schedule to be here. I hope that all of the participants enjoy the Conference and also enjoy Tokyo, a city with lots of fun and excitement. Best regards, Masanori Hatakeyama, M.D., Ph.D. Organizer 1st International Symposium on Carcinogenic Spiral 9th International Conference on Protein Phosphatase 2 General Information Congress 1st International Symposium on Carcinogenic Spiral & 9th International Conference on Protein Phosphatase Date February 1 (Tue) – 3 (Thu), 2011 Venue Tetsumon Memorial Hall Hongo Campus, The University of Tokyo 14th floor of Faculty of Medicine Experimental Research Bldg. -
Nod2-Independent Mechanism Bacteria Is Mediated by a TLR- And
IFN Regulatory Factor 3-Dependent Induction of Type I IFNs by Intracellular Bacteria Is Mediated by a TLR- and Nod2-Independent Mechanism This information is current as of September 27, 2021. Silvia Stockinger, Benjamin Reutterer, Barbara Schaljo, Carola Schellack, Sylvia Brunner, Tilo Materna, Masahiro Yamamoto, Shizuo Akira, Tadatsugu Taniguchi, Peter J. Murray, Mathias Müller and Thomas Decker J Immunol 2004; 173:7416-7425; ; Downloaded from doi: 10.4049/jimmunol.173.12.7416 http://www.jimmunol.org/content/173/12/7416 http://www.jimmunol.org/ References This article cites 75 articles, 41 of which you can access for free at: http://www.jimmunol.org/content/173/12/7416.full#ref-list-1 Why The JI? Submit online. • Rapid Reviews! 30 days* from submission to initial decision • No Triage! Every submission reviewed by practicing scientists by guest on September 27, 2021 • Fast Publication! 4 weeks from acceptance to publication *average Subscription Information about subscribing to The Journal of Immunology is online at: http://jimmunol.org/subscription Permissions Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Email Alerts Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts The Journal of Immunology is published twice each month by The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2004 by The American Association of Immunologists All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. The Journal of Immunology IFN Regulatory Factor 3-Dependent Induction of Type I IFNs by Intracellular Bacteria Is Mediated by a TLR- and Nod2-Independent Mechanism1 Silvia Stockinger,2* Benjamin Reutterer,2* Barbara Schaljo,* Carola Schellack,† Sylvia Brunner,† Tilo Materna,* Masahiro Yamamoto,§ Shizuo Akira,§ Tadatsugu Taniguchi,¶ Peter J. -
Loss of Transcription Factor IRF-1 Affects Tumor Susceptibility in Mice Carrying the Ha- Ras Transgene Or Nullizygosity for P53
Downloaded from genesdev.cshlp.org on September 26, 2021 - Published by Cold Spring Harbor Laboratory Press RESEARCH COMMUNICATION Accumulating evidence has also suggested that IRF-1 Loss of transcription factor controls tumor susceptibility. Transformed phenotypes IRF-1 affects tumor of c-myc-orfosB-expressing cells, for example, can be susceptibility in mice carrying suppressed by ectopic expression of IRF-1 (Tanaka et al. 1994b). Furthermore, unlike primary mouse embryonic the Ha-ras transgene fibroblasts (MEFs) from wild-type mice, MEFs from mu- or nullizygosity for p53 tant mice homozygous for IRF-1 deficiency undergo transformation upon expression of an activated form of Hiroaki Nozawa,1,2 Eri Oda,1 Kazuki Nakao,3 c-Ha-ras (Tanaka et al. 1994a). In addition, IRF-1 is es- Masahiko Ishihara,1 Seiji Ueda,1 Taeko Yokochi,1 sential to DNA damage-induced apoptosis in proliferat- Kouetsu Ogasawara,1 Yoko Nakatsuru,4 ing T lymphocytes and MEFs expressing an activated Seiichiro Shimizu,4 Yoshikazu Ohira,4 form of c-Ha-ras (Tanaka et al. 1994a; Tamura et al. 1995). Interestingly, IRF-1 also regulates DNA damage- Kyoji Hioki,5 Shinichi Aizawa,6 induced cell cycle arrest in collaboration with the tumor Takatoshi Ishikawa,4 Motoya Katsuki,3 2 1 suppressor p53 through transcriptional activation of the Tetsuichiro Muto, Tadatsugu Taniguchi, p21WAF1/CIP1 gene (Tanaka et al. 1996). 1,7 and Nobuyuki Tanaka The human IRF-1 gene has been mapped to 5q31.1 1Department of Immunology, 2Department of Surgical (Willman et al. 1993). Genetic as well as epigenetic al- Oncology, and 4Department of Pathology, Graduate School terations in IRF-1 gene expression have been reported in of Medicine and Faculty of Medicine, University of Tokyo, human cancers. -
Aryl Hydrocarbon Receptor Suppresses Intestinal Carcinogenesis in Apcmin/؉ Mice with Natural Ligands
Aryl hydrocarbon receptor suppresses intestinal carcinogenesis in ApcMin/؉ mice with natural ligands Kaname Kawajiria,1, Yasuhito Kobayashib, Fumiaki Ohtakec,d, Togo Ikutaa, Yoshibumi Matsushimaa, Junsei Mimurae, Sven Petterssonf, Richard S. Pollenzg, Toshiyuki Sakakih, Takatsugu Hirokawai, Tetsu Akiyamad, Masafumi Kurosumib, Lorenz Poellingerj, Shigeaki Katoc,d, and Yoshiaki Fujii-Kuriyamac,e aResearch Institute for Clinical Oncology and bHospital, Saitama Cancer Center, 818 Komuro, Ina, Saitama, 362-0806, Japan; cExploratory Research for Advanced Technology and Solution Oriented Research for Science and Technology, Japan Science and Technology Agency, 4-1-8 Honcho, Kawaguchi, Saitama, 332-0012, Japan; dInstitute of Molecular and Cellular Biosciences, University of Tokyo, 1-1-1 Yayoi, Bunkyo-ku, Tokyo, 113-0032, Japan; eTsukuba Advanced Research Alliance Center, University of Tsukuba, Tennodai, Tsukuba, Ibaraki, 305-8577, Japan; fGerm-Free Facility and jDepartment of Cell and Molecular Biology, Karolinska Institute, S-171 77 Stockholm, Sweden; gDepartment of Biology, University of South Florida, Tampa, FL 33620; hDepartment of Biotechnology, Toyama Prefectural University, 5180 Kurokawa, Imizu, Toyama, 939-0398, Japan; and iComputational Biology Research Center, National Institute of Advanced Industrial Science and Technology, 2-42 Aomi, Koto-ku, Tokyo, 135-0064, Japan Edited by Tadatsugu Taniguchi, University of Tokyo, Tokyo, Japan, and approved June 23, 2009 (received for review February 26, 2009) Intestinal cancer is one of the most common human cancers. reported for some tumor suppressor gene products, such as VHL Aberrant activation of the canonical Wnt signaling cascade, for (11) and adenomatous polyposis coli (APC) (12). Also, the example, caused by adenomatous polyposis coli (APC) gene mu- natural AhR ligands of indole derivatives (13, 14), such as tations, leads to increased stabilization and accumulation of indole-3-acetic acid (IAA, so-called plant auxin), indole-3- -catenin, resulting in initiation of intestinal carcinogenesis. -
Class of Cytokines and the IFN Regulatory Factor (IRF) Transcription Factor Family
Downloaded from http://cshperspectives.cshlp.org/ on October 6, 2021 - Published by Cold Spring Harbor Laboratory Press The Interferon (IFN) Class of Cytokines and the IFN Regulatory Factor (IRF) Transcription Factor Family Hideo Negishi,1 Tadatsugu Taniguchi,1,2 and Hideyuki Yanai1,2 1Department of Molecular Immunology, Institute of Industrial Science, The University of Tokyo, Komaba 4-6-1, Meguro-ku, Tokyo 153-8505, Japan 2Max Planck-The University of Tokyo Center for Integrative Inflammology, Komaba 4-6-1, Meguro-ku, Tokyo 153-8505, Japan Correspondence: [email protected] Interferons (IFNs) are a broad class of cytokines elicited on challenge to the host defense and are essential for mobilizing immune responses to pathogens. Divided into three classes, type I, type II, and type III, all IFNs share in common the ability to evoke antiviral activities initiated by the interaction with their cognate receptors. The nine-member IFN regulatory factor (IRF) family, first discovered in the context of transcriptional regulation of type I IFN genes follow- ing viral infection, are pivotal for the regulation of the IFN responses. In this review, we briefly describe cardinal features of the three types of IFNs and then focus on the role of the IRF family members in the regulation of each IFN system. ll three classes of interferons (IFNs) are so quenced, and formally recognized to comprise a Anamed because of the shared property to related gene family (Knight 1975; Taniguchi interfere with viral replication in the host et al. 1979; Maeda et al. 1980; Rubinstein et al. (Weissmann and Weber 1986; Taniguchi 1988; 1981; Weissmann and Weber 1986; Taniguchi Stark et al. -
Tadatsugu Taniguchi, Ph.D. Present Position and Address
CURRICULUM VITAE (February 9, 2015) Tadatsugu Taniguchi, Ph.D. Present Position and Address: Project Professor, Department of Molecular Immunology, Institute of Industrial Science, University of Tokyo Director, Max Planck-The University of Tokyo Center for Integrative Inflammology E-mail: [email protected] Educational Background: 1971: B. Sci. in Biology, Tokyo University of Education, Tokyo, Japan 1978: Ph.D. in Molecular Biology, University of Zurich, Zurich, Switzerland Professional Experience: 1972 - 1974: Borsa di Studio (Research Fellow), Laboratory of Biological Chemistry, University of Naples, Naples, Italy 1974 - 1978: Forschungs-Assistent (Research Assistant), University of Zurich, Zurich, Switzerland 1978 - 1980: Associate, Department of Biochemistry, Cancer Institute, Japanese Foundation for Cancer Research, Tokyo, Japan 1980 - 1983: Associate Member, Department of Biochemistry, Cancer Institute, Japanese Foundation for Cancer Research 1980 - 1982: Visiting Associate Professor, New York University Medical Center, New York, U.S.A. 1983 - 1984: Member and Chief, Department of Biochemistry, Cancer Institute, Japanese Foundation for Cancer Research 1984 - 1994: Professor, Division of Molecular Biology, Institute for Molecular and Cellular Biology, Osaka University 1995 - 1997: Professor, Department of Immunology, Faculty of Medicine, The University of Tokyo 1997 - 2012: Professor, Department of Immunology, Graduate School of Medicine and Faculty of Medicine, The University of Tokyo 1998-2000: Member of the Science Council, Ministry of Education, Culture, Sports, and Science of Japan. 2002-2008: Co-chair person, International Affairs Committee, American Association for Cancer Research 2003-present Foreign Associate Member, National Academy of Sciences, U.S.A. 2005-present Member of the Science Council of Japan 2006-present Visiting Professor, Wakayama Medical University 2006-present Adjunct Professor, New York University Medical School, U.S.A. -
A NOTE from the ICIS PRESIDENT, TADATSUGU TANIGUCHI Dear Colleagues and Friends
In This Issue: In Remembrance p2 2015 ICIS Awardees p5 Vilcek Prize p13 New Members p15 Aging & Inflammation by Annette Khalid p19 Discovery of IFN-gamma by Julius Youngner p21 ICIS Committee Minutes p27 Cytokines 2016, 2017 p32 SignalTHE INTERNATIONAL CYTOKINE AND INTERFERON SOCIETYsNEWSLETTER APRIL 2016 I VOLUME 4 I NO. 1 A NOTE FROM THE ICIS PRESIDENT, TADATSUGU TANIGUCHI Dear Colleagues and Friends, As the incoming President of the ICIS, I would first and foremost like There is no question that understanding cytokine biology can impact to thank my close friend Richard Flavell for his service as President all aspects of medicine, from cancer to autoimmune disease to of the society for the past two years. It was indeed a new era for the neural development and function. Thus, the ICIS shall serve as a ICIS, as under Richard’s leadership the cultures of two societies common ground where scientists interested in all aspect of cytokine were joined. I will no doubt call upon the advice of Richard and biology can join and work together to better human health. On the members of the ICIS Council during my term of office. I am eager to other hand, the challenging climate of research funding has placed continue the growth and success of the society, particularly as it new demands and strains on our desire to have a vibrant and faces new challenges. meaningful organization. It has always been the aim of the ICIS to When I started working on cytokines, namely on the isolation and keep dues low and make membership affordable for scientists at all characterization of interferon- gene in 1978, the term “cytokine” levels, from graduate students to Full Professors. -
Japan's Post-War Pharmaceutical Industry, 1945
Unrealised Potential: Japan’s Post-war Pharmaceutical Industry, 1945-2005 Maki Umemura A thesis submitted to the Department of Economic History London School of Economics and Political Science Candidate for the degree of Doctor of Philosophy London, August 2008 UMI Number: U61B404 All rights reserved INFORMATION TO ALL USERS The quality of this reproduction is dependent upon the quality of the copy submitted. In the unlikely event that the author did not send a complete manuscript and there are missing pages, these will be noted. Also, if material had to be removed, a note will indicate the deletion. Dissertation Publishing UMI U613404 Published by ProQuest LLC 2014. Copyright in the Dissertation held by the Author. Microform Edition © ProQuest LLC. All rights reserved. This work is protected against unauthorized copying under Title 17, United States Code. ProQuest LLC 789 East Eisenhower Parkway P.O. Box 1346 Ann Arbor, Ml 48106-1346 1K£S£S f nig ■ i and EconomicS o b ** - Declaration I certify that the thesis I have presented for examination for the MPhil/PhD degree of the London School of Economics and Political Science is my own work. 28 August 2008 Abstract Japan’s existing pharmaceutical industry was devastated in the Second World War. But the industry recovered quickly, and in 1963, Japan had become the second largest producer of pharmaceuticals after the United States. Unlike its automobile or electronics industries, however, Japan’s pharmaceutical industry did not become a global leader. Japan remains a net importer of pharmaceuticals and few Japanese drugs are found outside of Japan. The global pharmaceutical industry is led by firms from the United States, the United Kingdom and Switzerland, rather than those from Japan.