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Biochemistrystanford00kornrich.Pdf
University of California Berkeley Regional Oral History Office University of California The Bancroft Library Berkeley, California Program in the History of the Biosciences and Biotechnology Arthur Kornberg, M.D. BIOCHEMISTRY AT STANFORD, BIOTECHNOLOGY AT DNAX With an Introduction by Joshua Lederberg Interviews Conducted by Sally Smith Hughes, Ph.D. in 1997 Copyright 1998 by The Regents of the University of California Since 1954 the Regional Oral History Office has been interviewing leading participants in or well-placed witnesses to major events in the development of Northern California, the West, and the Nation. Oral history is a method of collecting historical information through tape-recorded interviews between a narrator with firsthand knowledge of historically significant events and a well- informed interviewer, with the goal of preserving substantive additions to the historical record. The tape recording is transcribed, lightly edited for continuity and clarity, and reviewed by the interviewee. The corrected manuscript is indexed, bound with photographs and illustrative materials, and placed in The Bancroft Library at the University of California, Berkeley, and in other research collections for scholarly use. Because it is primary material, oral history is not intended to present the final, verified, or complete narrative of events. It is a spoken account, offered by the interviewee in response to questioning, and as such it is reflective, partisan, deeply involved, and irreplaceable. ************************************ All uses of this manuscript are covered by a legal agreement between The Regents of the University of California and Arthur Kornberg, M.D., dated June 18, 1997. The manuscript is thereby made available for research purposes. All literary rights in the manuscript, including the right to publish, are reserved to The Bancroft Library of the University of California, Berkeley. -
Suppression of Oncogenic Ras by Mutant Neurofibromatosis Type 1 Genes with Single Amino Acid Substitutions
Proc. Natl. Acad. Sci. USA Vol. 90, pp. 6706-6710, July 1993 Biochemistry Suppression of oncogenic Ras by mutant neurofibromatosis type 1 genes with single amino acid substitutions MASATO NAKAFUKU*t, MASARU NAGAMINE*, AKIHIRA OHTOSHI*, KAZUMA TANAKAO§, AKIo TOH-E*, AND YOSHITO KAZIRO*¶ *DNAX Research Institute of Molecular and Cellular Biology, Palo Alto, CA 94304-1104; and tDepartment of Biology, Faculty of Science, University of Tokyo, Tokyo 113, Japan Communicated by Paul Berg, April 1, 1993 ABSTRACT NFI was frit identified as the gene responsible growth through the regulation of adenylate cyclase (14, 15). for the pathogenesis of the human genetic disorder neurofibro- Thus, yeast cells carrying activated mutations in Ras (such as matosis type 1. cDNA cloning revealed that its putative protein [Val'9]Ras2 and [Leua]Ras2) are defective in responding to product has a domain showing signfifcant sequence homology environmental conditions and show a variety of phenotypes with the mammalian Ras GTPase activating protein and two including a heat-shock-sensitive phenotype (14, 15). yeast Saccharomyces cerevisiae proteins, Iral and Ira2. The Ras S. cerevisiae also possesses two NF1 homologs, Iral and GTPase activating protein-related domain of the NFI gene Ira2, and human NF1 is structurally closer to yeast Ira than product (NF1-GRD) stimulates GTPase activity of normal Ras to human GAP (1-4). NF1 and Ira are also functionally proteins but not of oncogenic mutant Ras from both mamma- related since NF1-GRD expressed in yeast cells can com- lian and yeast cells. Thus, in yeast, NF1-GRD can suppress the plement ira-deficient yeast. -
Suzanne Pfeffer
July 2010 ASBMB PreSidentiAl PriMer: Suzanne Pfeffer American Society for Biochemistry and Molecular Biology AAdjuvdjuvAAntnt IImmunothermmunotherAApypy ususIIngng KKrnrn70007000 KRN7000 (α-Galactosyl Ceramide) Avanti Number 867000 Supplier: Funakoshi Co. Ltd. Hepatic metastasis is a major clinical problem in cancer treatment. We examined antitumor ac- tivity of alpha-galactosylceramide (KRN7000) on mice with spontaneous liver metastases of re- ticulum cell sarcoma M5076 tumor cells (spontaneous metastasis model). In this model, all mice that were s.c. challenged with one million tumor cells developed a solid s.c. mass by day 7 and died of hepatic metastases. In the current study, we administered 100 microg/kg of KRN7000 to the model mice on days 7, 11, and 15. This treatment suppressed the growth of established liver metastases and resulted in the prolongation of survival time. Fluorescence-activated cell sorter analysis of phenotypes of spleen cells, hepatic lymphocytes, and regional lymph node cells around the s.c. tumor revealed that CD3+NK1.1+ (NKT) cells increased in hepatic lym- phocytes of the KRN7000-treated mice. Cytotoxic activity and IFN-gamma production of hepatic lymphocytes were augmented in comparison with those of spleen cells and regional LN cells. At the same time, interleukin (IL)-12 production of hepatic lymphocytes was markedly enhanced. Neutralization of IL-12 using a blocking monoclonal antibody diminished the prolonged survival time. These results showed that the in vivo antitumor effects of KRN7000 on spontaneous liver metastases were dependent on the endogenous IL-12 production, where NKT cells in the liver are suggested to be involved. Adjuvant immunotherapy using KRN7000 could be a promising modality for the prevention of postoperative liver metastases. -
NIH Conflict of Interest Regs Revised
OCTOBEROCTOBER 2005 www.asbmb.org Constituent Society of FASEB AMERICAN SOCIETY FOR BIOCHEMISTRY AND MOLECULAR BIOLOGY NIH Conflict of Interest Regs Revised SEE PAGE 30 FOR NEW CLARA BENSON TRAVEL FELLOWSHIP AWARD Held in conjunction with EB2006 Custom Antibodies Your Way! Choose the protocol that is right for you! QwikScreen ™: 65 day, 2 rabbit protocol - 4 immunizations, 3 bleeds/rabbit (~100ml serum), customer supplied peptide/protein - Options: Peptide synthesis, immunograde Conjugation to carrier u ELISA u u Animal extensionsMS analysis $685 Standard: 80 day, 2 rabbit protocol - 5 immunizations, 5 bleeds/rabbit (~ 200ml ser Options: um), ELISA, customer supplied peptide/pr Peptide synthesis MS Check™ peptide sequence confirmation u HPLC purified peptide Affinity purification otein - Pinnacle: $975 u HPLC and MS analysis u Complete Affinity Purified Protocol- Animal extensions 2 rabbit pr 5 bleeds/rabbitotocol, (~ 200mlepitope serum), design, peptide PhD technical synthesis support, (up to 20mer),5 immunizations, HPLC purified to ~85%, 5+mg peptide to customer, ELISA, evaluation period, affinity purification, and morMS Check™ peptide sequence confirmationNo Hidden Charges! e… - Discounts for Multiple Protocols$1795 , Includes peptide sequencing by CID MS/MS– u Guaranteed Peptide Let our enthusiasm for scienceExpert workTechnical for SupportFidelity! P: 508.303.8222 www.21stcenturybio.com Toll-free: 877.217.8238 F: 508.303.8333 you! E: [email protected] www.asbmb.org AMERICAN SOCIETY FOR BIOCHEMISTRY AND MOLECULAR BIOLOGY OCTOBER -
Colony-Stimulating Factor
Proc. Natl. Acad. Sci. USA Vol. 83, pp. 7633-7637, October 1986 Biochemistry Isolation and characterization of the cDNA for murine granulocyte colony-stimulating factor (murine fibrosarcoma NFSA cells/cDNA sequence/protein homology/growth factor/differentiation) MASAYUKI TSUCHIYA, SHIGETAKA ASANO, YOSHITo KAZIRO, AND SHIGEKAZU NAGATA Institute of Medical Science, University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 108, Japan Communicated by Charles Yanofsky, June 26, 1986 ABSTRACT A cDNA sequence coding for murine granu- In this report, we describe the isolation of the murine locyte colony-stimulating factor (G-CSF) has been isolated G-CSF cDNA from a recombinant X phage library prepared from a cDNA library prepared with mRNA derived from from the murine fibrosarcoma NFSA cell line, which pro- murine fibrosarcoma NFSA cells, which produce G-CSF con- duces G-CSF constitutively. The murine G-CSF cDNA was stitutively. Identification of murine G-CSF cDNA was based on identified by using cross-hybridization with human G-CSF the cross-hybridization with human G-CSF cDNA under a cDNA under a low-stringency condition. The cDNA was low-stringency condition. The cDNA can encode a polypeptide expressed in monkey COS cells under the simian virus 40 consisting of a 30-amino acid signal sequence, followed by a (SV40) early promoter. The protein produced by COS cells mature G-CSF sequence of 178 amino acids with a calculated had an ability to stimulate the granulocyte colony formation Mr of 19,061. The nucleotide sequence and the deduced amino in bone marrow cells and to support the proliferation of acid sequence of murine G-CSF cDNA were 69.3% and 72.6% murine NFS-60 myeloid leukemic cells. -
Thrombin-Induced Inhibition of Myoblast Differentiation Is Mediated
FEBS 23593 FEBS Letters 472 (2000) 297^301 CORE Metadata, citation and similar papers at core.ac.uk Provided by Elsevier - Publisher Thrombin-inducedConnector inhibition of myoblast di¡erentiation is mediated by GLQ Motoshi Nagao, Yoshito Kaziro, Hiroshi Itoh* Faculty of Bioscience and Biotechnology, Tokyo Institute of Technology, 4259 Nagatsuta-cho, Midori-ku, Yokohama 226-8501, Japan Received 17 March 2000 Edited by Julio Celis an important role in skeletal muscle development. It has been Abstract Thrombin has been shown to inhibit skeletal muscle differentiation. However, the mechanisms by which thrombin shown that thrombin is involved in synapse elimination occur- represses myogenesis remain unknown. Since the thrombin ring at the neuromuscular junction during muscle develop- ment [9,10]. In addition, thrombin causes a delay in skeletal receptor couples to Gi,Gq=11 and G12, we examined which subunits of heterotrimeric guanine nucleotide-binding regulatory myogenesis [4^7]. The thrombin receptor is expressed in cul- proteins (GKi,GKq=11,GK12 or GLQLQ) participate in the thrombin- tured myoblasts and its expression decreases once the myo- induced inhibition of C2C12 myoblast differentiation. GKi2 and blasts fuse to form multinucleated myotubes [5]. Thrombin GK11 had no inhibitory effect on the myogenic differentiation. has been reported to act as a mitogen in myoblasts as well GK12 prevented only myoblast fusion, whereas GLQLQ inhibited both as ¢broblasts and smooth muscle cells, and induce their pro- the induction of skeletal muscle-specific markers and the liferation [4,5]. In contrast, it has been reported that thrombin myotube formation. In addition, the thrombin-induced reduction does not induce a mitogenic signal in myoblastic cell line [6], of creatine kinase activity was blocked by the C-terminal peptide of L-adrenergic receptor kinase, which is known to sequester free and that it inhibits myoblast apoptosis and functions as a GLQLQ. -
Giant Gene Thieves Have You Renewed Your Membership for 2020?
Vol. 18 / No. 10 / November 2019 THE MEMBER MAGAZINE OF THE AMERICAN SOCIETY FOR BIOCHEMISTRY AND MOLECULAR BIOLOGY Giant gene thieves Have you renewed your membership for 2020? Together, we’ll continue to advocate for science, connect researchers around the world and build a bright future for biochemists and molecular biologists everywhere. Learn more at www.asbmb.org/membership CONTENTS NEWS FEATURES PERSPECTIVES 2 24 50 GIANT GENE THIEVES SERVICE BEYOND SCIENCE EDITOR’S NOTE ese viruses are changing what we know Weaving social innovation and scienti c It’s about time about structural and evolutionary biology methods for a bright future 3 32 MEMBER UPDATE MEET SEAN DAVIDSON 7 e JLR associate editor rethinks cholesterol NEW MEMBERS 9 24 YEAR OF (BIO)CHEMICAL ELEMENTS For November, it’s that smell of sulfur 10 NEWS Bacterial invasion may explain recurrent urinary tract infections 11 13 JOURNAL NEWS 11 Snug as a bug in the mud 50 13 Researchers clock DNA’s recovery time 14 Lack of sleep a ects fat metabolism 15 is protein makes antibody drugs work 16 From the journals 22 LIPID NEWS Phospholipids and innate immunity 32 2020 Award Winners … page 37 Ruth Kirschstein Diversity in Science Award: ASBMB Award for Exemplary Contributions to Lizabeth Allison Education: Paul Black Herbert Tabor Research Award: Kevin Campbell Bert and Natalie Vallee Award: Edward Dennis ASBMB–Merck Award: Manajit Hayer–Hartl Alice and C. C. Wang Award in Molecular Parasitology: Patricia Johnson Avanti Award in Lipids: Jean Schaff er Earl and Thressa Stadtman Young Scholar Award: William C. Rose Award: Celia Schiff er David Pagliarini DeLano Award for Computational Biosciences: Mildred Cohn Award in Biological Chemistry: ANNUAL MEETING Yang Zhang Carol Fierke Walter Shaw Young Investigator Award in Lipids: Jeremy Baskin NOVEMBER 2019 ASBMB TODAY 1 EDITOR’S NOTE THE MEMBER MAGAZINE OF THE AMERICAN SOCIETY FOR BIOCHEMISTRY AND MOLECULAR BIOLOGY It’s about time OFFICERS COUNCIL MEMBERS Gerald Hart Suzanne Barbour By Comfort Dorn President Joan Broderick Matt Gentry Toni M. -
Protein Kinase Activation
SEE INSIDE FOR 2008 ANNUAL MEETING SESSION OVERVIEWS July 2007 Protein Kinase Activation American Society for Biochemistry and Molecular Biology POSTDOCTORAL FELLOWSHIP Department of Dermatology, OHSU, Portland, Oregon Training Program in Molecular Basis of Skin Pathobiology Promoting Understanding Position for recent PhD, MD/PhD or MD (US citizen or Permanent Resident) in NIH-funded program for training highly of the Molecular Nature qualifi ed candidates for academic careers in basic & translational research in skin diseases, including cancer & psoriasis. OHSU Dermatology has a strong history of clinical & scientifi c of Life Processes research & a 40-year record in training dermatology residents including physician scientists & postdoctoral scientists on the path to independence. Features of this training program are a core of Dermatology faculty & a multidisciplinary network of scientists with international recognition in areas highly relevant to epithelial cell fate, development & diseases. The training program includes seminars in mentors’ departments, Dermatology Research Division meetings & symposia, research forums tailored to postdoctoral students, & national/international meetings in cutaneous biology. Successful candidates desiring an academic career in basic or translational research in cancer The Society’s purpose is to or investigative dermatology using surface epithelial models can advance the science of bio- expect to receive training toward independence in research with chemistry & molecular biology a strong clinical translational -
CHEMISTRY NEWS UNIVERSITY of OREGON COLLEGE of ARTS and SCIENCES DEPARTMENT of CHEMISTRY 1996 from the DEPARTMENT HEAD the Past Year Was an Exhilarat- Didates
CHEMISTRY NEWS UNIVERSITY OF OREGON COLLEGE OF ARTS AND SCIENCES DEPARTMENT OF CHEMISTRY 1996 FROM THE DEPARTMENT HEAD The past year was an exhilarat- didates. We did something un- ing one for the Department of heard offor Oregon anywaywe Chemistry. Among many exciting requested permission to hire both things that happened, we hired candidates. To our mild surprise, two new faculty members, our the deans office and the Graduate Achievement Endowment Fund School agreed this was an opportu- continues to grow, we honored nity we should not miss. We hired three distinguished alumni with both Andy Marcus and Mark achievement awards, members of Lonergan. Im sure it is obvious our faculty were recognized with that the administration wouldnt national and local awards, and we do this for just any department. It graduated thirty-eight enthusiastic is a sign of our departments undergraduate and graduate stu- strength and quality that we were dents. Let me briefly recount these permitted to hire two new faculty events and achievements. members. Last fall we ran a search for a One of the reasons our depart- physical chemist to replace Warner ment remains optimistic about the Peticolas, who retired. We inter- future is that we have generous viewed four candidates and found alumni who contribute to our © JACK LIU ourselves having to decide be- growing Achievement Endowment tween two absolutely superb can- continued on page 2 Chemistry Commencement Gets Personal Remember when the only and friends. In a new twist this graduation event was a large gath- year, students wrote a humorous ering on a football field? Times script, Our Seniors Top Ten List have changed. -
Hatzios Thesis Formatted
Investigations of Metabolic Pathways in Mycobacterium tuberculosis by Stavroula K Hatzios A dissertation submitted in partial satisfaction of the requirements for the degree of Doctor of Philosophy in Chemistry in the Graduate Division of the University of California, Berkeley Committee in charge: Professor Carolyn R. Bertozzi, Chair Professor Matthew B. Francis Professor Tom Alber Fall 2010 Investigations of Metabolic Pathways in Mycobacterium tuberculosis © 2010 By Stavroula K Hatzios Abstract Investigations of Metabolic Pathways in Mycobacterium tuberculosis by Stavroula K Hatzios Doctor of Philosophy in Chemistry University of California, Berkeley Professor Carolyn R. Bertozzi, Chair Mycobacterium tuberculosis (Mtb), the bacterium that causes tuberculosis in humans, infects roughly two billion people worldwide. However, less than one percent of infected individuals are symptomatic. Most have a latent infection characterized by dormant, non- replicating bacteria that persist within a mass of immune cells in the lung called the granuloma. The granuloma provides a protective barrier between infected cells and surrounding tissue. When host immunity is compromised, the granuloma can deteriorate and reactivate the disease. In order to mount a latent infection, Mtb must survive in alveolar macrophages, the host’s primary line of defense against this intracellular pathogen. By evading typical bactericidal processes, Mtb is able to replicate and stimulate granuloma formation. The mechanisms by which Mtb persists in macrophages are ill defined; thus, elucidating the factors responsible for this hallmark of Mtb pathogenesis is an important area of research. This thesis explores three discrete metabolic pathways in Mtb that are likely to mediate its interactions with host immune cells. The first three chapters examine the sulfate assimilation pathway of Mtb and its regulation by the phosphatase CysQ. -
1968 Commencement Program
UNIVERSITY of PENNSYLVANIA - Two Hundred and Twelfth Commencement for the Conferring of Degrees PHILADELPHIA CIVIC CENTER Monday, May 20, 1968 10:00 A.M. jJ STAGE (1, ......II ,........I " Official Guests Medicine College for Women Graduate Medicine Wharton Law College Nursing Graduate Allied Fine Arts Medical Professions Dental Medicine Veterinary Medicine Wharton Graduate Graduate Arts& Sciences Civil& Mechanical Engineering Chemical Graduate Engineering Education Electrical Engineering Social Work Metallurgy Annenberg Guests will find this diagram helpful in locating the opposite page under Degrees in Course. Reference approximate seating of the degree candidates. The to the paragraph on page seven describing the seating and the order of march in the student pro colors of the candidates' hoods according to their cession correspond closely to the order by school fields of study may further assist guests in placing in which the candidates for degrees are presented. the locations of the various schools. This sequence is shown in the Contents on the Contents Page Seating Diagram of the Graduating Students .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. 2 The Commencement Ceremony . 4 Background of the Ceremonies . .. .. .. 6 Degrees in Course . .. .. .. 8 The College of Arts and Sciences . 8 The Engineering Schools . .. .. .. 14 The Towne School of Civil and Mechanical Engineering ... ........ ......... 14 The School of Chemical Engineering . .. .. .. 15 The Moore School of Electrical Engineering . .. 16 The School of Metallurgy and Materials Science . .. .. 18 The Wharton School of Finance and Commerce . 19 The College of Liberal Arts for Women ....... .. ... ...... .. .. .... ............ ..... .. ......... 26 The School of Nursing ... ........................... .... ................ ... ................... ........ 31 The School of Allied Medical Professions . .. .. 3 3 The Graduate School of Arts and Sciences . .. .. .. 34 The School of Medicine . -
Regulation of Smooth Muscle A-Actin Promoter in Ras-Transformed Cells: Usefulness for Setting up Reporter Gene-Based Assay System for Drug Screening
[CANCER RESEARCH 52, 6877-6884, December 15, 1992] Regulation of Smooth Muscle a-Actin Promoter in ras-transformed Cells: Usefulness for Setting Up Reporter Gene-based Assay System for Drug Screening C. Chandra Kumar, ~ Pierre Bushel, Sheela Mohan-Peterson, 2 and Fernando Ramirez Department of Tumor Biology, Schering-Plough Research Institute, Bloomfield, New Jersey 07003 ABSTRACT cancer have impaired GTPase activity, are insensitive to GAP, and remain bound to GTP leading to uncontrolled cell growth Oncogenic activation of ras results in changes in the transcription of (6). In addition, a number of posttranslational modifications of several genes leading to uncontrolled cell growth. In this paper, we ras such as palmitoylation, farnesylation, proteolytic cleavage, demonstrate that transformation of fibroblast cells by the ras oncogene leads to transcriptional repression of the smooth muscle a-actin pro- and carboxymethylation have been found to be essential for moter. Transient transfection analysis of plasmids containing the 5' biological activity of ras (9-11). upstream region of the human a-actin gene fused to human growth A number of approaches are being taken to find drugs that hormone or bacterial chloramphenicol acetyltransferase coding se- inhibit the accumulation of the GTP-bound form of the ras p21 quences into Rat-2 and ras-transformed Rat-2 (HO6) cells indicates that protein. These include assay systems designed to identify drugs a-actin promoter is repressed in ras-transformed cells. In addition, that inhibit the nucleotide exchange activity of ras, or stimulate stable rat fibroblast cell lines expressing human growth hormone or the GTPase activity of mutant ras, or inhibit ras:GAP interac- B-galactosidase under the control of ~,-actin promoter exhibit repressed tion, etc.