Viral Nanotechnology
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Oncogenes of DNA Tumor Viruses1
[CANCER RESEARCH 48. 493-496. February I. 1988] Perspectives in Cancer Research Oncogenes of DNA Tumor Viruses1 Arnold J. Levine Department of Molecular Biology, Princeton University, Princeton, New Jersey 08544 Experiments carried out over the past 10-12 years have the cellular oncogenes. It will attempt to identify where more created a field or approach which may properly be termed the information is required or contradictions appear in the devel molecular basis of cancer. One of its major accomplishments oping concepts. Finally, this communication will examine ex has been the identification and understanding of some of the amples of cooperation between oncogenes and other gene prod functions of a group of cancer-causing genes, the oncogenes. ucts which modify the mode of action of the former. If we are The major path to the oncogenes came from the study of cancer- on the right track, then general principles may well emerge. causing viruses. The oncogenes have been recognized and stud Tumor formation in animals or transformation in cell culture ied by two separate but related groups of virologists focusing has been demonstrated with many different DNA-containing upon either the DNA (1) or RNA (2) tumor viruses (they even viruses (1). In most cases it has been possible to identify one or have separate meetings now that these fields have grown so a few viral genes and their products that are responsible for large). From their studies it has become clear that the oncogenes transformation or, in some cases, tumorigenesis. A list of these of each virus type have very different origins. -
Tätigkeitsbericht 2007/2008
Tätigkeitsbericht 2007/2008 8 200 / 7 0 20 Tätigkeitsbericht Stiftung bürgerlichen Rechts Martinistraße 52 · 20251 Hamburg Tel.: +49 (0) 40 480 51-0 · Fax: +49 (0) 40 480 51-103 [email protected] · www.hpi-hamburg.de Impressum Verantwortlich Prof. Dr. Thomas Dobner für den Inhalt Dr. Heinrich Hohenberg Redaktion Dr. Angela Homfeld Dr. Nicole Nolting Grafik & Layout AlsterWerk MedienService GmbH Hamburg Druck Hartung Druck + Medien GmbH Hamburg Titelbild Neu gestaltete Fassade des Seuchenlaborgebäudes Tätigkeitsbericht 2007/2008 Heinrich-Pette-Institut für Experimentelle Virologie und Immunologie an der Universität Hamburg Martinistraße 52 · 20251 Hamburg Postfach 201652 · 20206 Hamburg Telefon: +49-40/4 80 51-0 Telefax: +49-40/4 80 51-103 E-Mail: [email protected] Internet: www.hpi-hamburg.de Das Heinrich-Pette-Institut ist Mitglied der Leibniz-Gemeinschaft (WGL) Internet: www.wgl.de Inhaltsverzeichnis Allgemeiner Überblick Vorwort ................................................................................................... 1 Die Struktur des Heinrich-Pette-Instituts .............................................. 2 Modernisierung des HPI erfolgreich abgeschlossen ............................ 4 60 Jahre HPI .............................................................................................. 5 Offen für den Dialog .............................................................................. 6 Preisverleihungen und Ehrungen .......................................................... 8 Personelle Veränderungen in -
Inhibition of HIV-1 by an Anti-Integrase Single-Chain Variable
Gene Therapy (1999) 6, 660–666 1999 Stockton Press All rights reserved 0969-7128/99 $12.00 http://www.stockton-press.co.uk/gt Inhibition of HIV-1 by an anti-integrase single-chain variable fragment (SFv): delivery by SV40 provides durable protection against HIV-1 and does not require selection M BouHamdan1, L-X Duan1, RJ Pomerantz1 and DS Strayer1,2 1The Dorrance H Hamilton Laboratories, Center for Human Virology, Division of Infectious Diseases, Department of Medicine; and 2Department of Pathology, Anatomy and Cell Biology, Jefferson Medical College, Thomas Jefferson University, Philadelphia, PA, USA Human immunodeficiency virus type I (HIV-1) encodes the SFv-IN was confirmed by Western blotting and several proteins that are packaged into virus particles. Inte- immunofluorescence staining, which showed that Ͼ90% of grase (IN) is an essential retroviral enzyme, which has SupT1 T-lymphocytic cells treated with SV(Aw) expressed been a target for developing agents to inhibit virus repli- the SFv-IN protein without selection. When challenged, cation. In previous studies, we showed that intracellular HIV-1 replication, as measured by HIV-1 p24 antigen expression of single-chain variable antibody fragments expression and syncytium formation, was potently inhibited (SFvs) that bind IN, delivered via retroviral expression vec- in cells expressing SV40-delivered SFv-IN. Levels of inhi- tors, provided resistance to productive HIV-1 infection in bition of HIV-1 infection achieved using this approach were T-lymphocytic cells. In the current studies, we evaluated comparable to those achieved using murine leukemia virus simian-virus 40 (SV40) as a delivery vehicle for anti-IN (MLV) as a transduction vector, the major difference being therapy of HIV-1 infection. -
Closer to the Heart: an Exploration of Caring and Creative Visual Arts Classrooms
University of Denver Digital Commons @ DU Electronic Theses and Dissertations Graduate Studies 1-1-2010 Closer to the Heart: An Exploration of Caring and Creative Visual Arts Classrooms Juli B. Kramer University of Denver Follow this and additional works at: https://digitalcommons.du.edu/etd Part of the Art Education Commons, Curriculum and Instruction Commons, and the Secondary Education Commons Recommended Citation Kramer, Juli B., "Closer to the Heart: An Exploration of Caring and Creative Visual Arts Classrooms" (2010). Electronic Theses and Dissertations. 852. https://digitalcommons.du.edu/etd/852 This Dissertation is brought to you for free and open access by the Graduate Studies at Digital Commons @ DU. It has been accepted for inclusion in Electronic Theses and Dissertations by an authorized administrator of Digital Commons @ DU. For more information, please contact [email protected],[email protected]. CLOSER TO THE HEART: AN EXPLORATION OF CARING AND CREATIVE VISUAL ARTS CLASSROOMS __________ A Dissertation Presented to the Morgridge College of Education University of Denver __________ In Partial Fulfillment of the Requirements for the Degree Doctor of Philosophy __________ by Juli B. Kramer June 2010 Advisor: P. Bruce Uhrmacher, Ph.D. ©Copyright by Juli B. Kramer 2010 All Rights Reserved Author: Juli B. Kramer Title: CLOSER TO THE HEART: AN EXPLORATION OF CARING AND CREATIVE VISUAL ARTS CLASSROOMS Advisor: P. Bruce Uhrmacher, Ph.D. Degree Date: June 2010 Abstract This study demonstrates how caring and creative secondary level visual arts classes facilitate the development of learning environments that enliven and expect the best of students; help them develop as autonomous and creative learners; provide them opportunities to care for others and the world around them; and keep them connected to their schools and education. -
Hepatitis B Virus X Protein Inhibits P53 Sequence-Specific DNA Binding
Proc. Nati. Acad. Sci. USA Vol. 91, pp. 2230-2234, March 1994 Medical Sciences Hepatitis B virus X protein inhibits p53 sequence-specific DNA binding, transcriptional activity, and association with transcription factor ERCC3 XIN WEI WANG*, KATHLEEN FORRESTER*, HEIDI YEH*, MARK A. FEITELSONt, JEN-REN GUI, AND CURTIS C. HARRIS*§ *Laboratory of Human Carcinogenesis, Division of Cancer Etiology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892; tDepartment of Pathology and Cell Biology, Jefferson Medical College, Philadelphia, PA 19107; and tDepartment of Molecular Biology and Biochemistry, Shanghai Cancer Institute, Shanghai, People's Republic of China. Communicated by Bert Vogelstein, December 27, 1993 (receivedfor review December 9, 1993) ABSTRACT Chronic active hepatitis caused by infection about the role of HBX in HCC development. In this report, with hepatitis B virus, a DNA virus, is a major risk factor for we present results consistent with the hypothesis that HBX human hepatocellular carcinoma. Since the oncogenicity of binds to p53 and abrogates its normal cellular functions. several DNA viruses is dependent on the interaction of their viral oncoproteins with cellular tumor-suppressor gene prod- MATERIAL AND METHODS ucts, we investigated the interaction between hepatitis B virus X protein (HBX) and human wild-type p53 protein. HBX Plasmids. Plasmid constructs encoding GST-p53-WT, con- complexes with the wild-type p53 protein and inhibits its taining glutathione S-transferase (GST) fused to human wild- sequence-specific DNA binding in vitro. HBX expresslin also type p53, and GST-p53-135Y, containing GST fused to the inhibits p53-mediated transcrptional activation in vivo and the mutant p53 containing a His -* Tyr mutation at codon 135, in vitro asoition of p53 and ERCC3, a general transcription were provided by Jon Huibregtse (National Cancer Institute) factor involved in nucleotide excision repair. -
PP2A-Dependent Disruption of Centrosome Replication and Cytoskeleton Organization in Drosophila by SV40 Small Tumor Antigen
Oncogene (2008) 27, 6334–6346 & 2008 Macmillan Publishers Limited All rights reserved 0950-9232/08 $32.00 www.nature.com/onc ORIGINAL ARTICLE PP2A-dependent disruption of centrosome replication and cytoskeleton organization in Drosophila by SV40 small tumor antigen S Kotadia1,LRKao1, SA Comerford2, RT Jones1, RE Hammer3 and TL Megraw1 1Department of Pharmacology, The Cecil and Ida Green Center for Reproductive Biology Sciences, The University of Texas Southwestern Medical Center at Dallas, Dallas, TX, USA; 2Department of Molecular Genetics, The Cecil and Ida Green Center for Reproductive Biology Sciences, The University of Texas Southwestern Medical Center at Dallas, Dallas, TX, USA and 3Department of Biochemistry, The Cecil and Ida Green Center for Reproductive Biology Sciences, The University of Texas Southwestern Medical Center at Dallas, Dallas, TX, USA Viruses of the DNA tumor virus family share the ability to cell-cycle and apoptosis regulation, viral oncoproteins transform vertebrate cells through the action of virus- transform cells. Investigation of DNA tumor virus encoded tumor antigens that interfere with normal cell oncoproteins has led to the identification of many physiology. They accomplish this very efficiently by fundamental mechanisms of tumor suppression (Lavia inhibiting endogenous tumor suppressor proteins that et al., 2003; Ahuja et al., 2005). By altering the activity control cell proliferation and apoptosis. Simian virus 40 of p53, retinoblastoma protein and serine/threonine (SV40) encodes two oncoproteins, large tumor antigen, protein phosphatase 2A (PP2A), three key tumor which directly inhibits the tumor suppressors p53 and Rb, suppressors, SV40 can cause tumor formation in and small tumor antigen (ST), which interferes with transgenic mouse models (Ahuja et al., 2005; Arroyo serine/threonine protein phosphatase 2A (PP2A). -
The Simian Virus 40 Large Tumor Antigen Activates Csrc and Requires Csrc for Full Neoplastic Transformation
ANTICANCER RESEARCH 30: 47-54 (2010) The Simian Virus 40 Large Tumor Antigen Activates cSrc and Requires cSrc for Full Neoplastic Transformation ROZANNE ARULANANDAM, MULU GELETU and LEDA RAPTIS Departments of Microbiology and Immunology and Pathology, Queen's University, Kingston, Ontario, K7L 3N6, Canada Abstract. Aim: To investigate the role of the cellular The effects of TAg on the Rb family proteins are thought to be protooncogene product, cSrc, in neoplastic transformation by exerted by regulating the activity of the E2F transcription factors. the large tumor antigen of simian virus 40 (TAg), the ability of There are eight known E2F proteins (E2F1-8), all of which TAg to increase cSrc activity was examined. Materials and possess a DNA-binding domain that governs their interactions Methods: cSrc activity was measured in cells expressing wild- with a common consensus sequence present in the promoters of type or mutant TAg and compared to the parental line. Results: a number of genes (reviewed in (4, 5)). In quiescent cells, E2F- The results indicated that TAg expression in mouse 3T3 regulated genes are not expressed because their promoters are fibroblasts causes a dramatic increase in cSrc activity, a finding occupied primarily by p130/E2F4 complexes which repress which establishes TAg as a cSrc activator. This ability transcription. Following receptor stimulation, Rb proteins are depended upon a TAg, intact retinoblastoma-susceptibility gene inactivated through phosphorylation by the cyclin-dependent product (Rb) family-binding site. In addition, genetic ablation kinases and this results in the replacement of the p130/E2F4 of pRb in mouse fibroblasts increased cSrc activity, suggesting complexes by the ‘activating’ E2F1-3. -
Identification of Rab18 As an Essential Host Factor for Bkpyv Infection Using a Whole Genome RNA 2 Interference Screen
bioRxiv preprint doi: https://doi.org/10.1101/157602; this version posted June 29, 2017. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-NC-ND 4.0 International license. 1 Identification of Rab18 as an Essential Host Factor for BKPyV Infection Using a Whole Genome RNA 2 Interference Screen 3 4 Linbo Zhaoa, Michael J. Imperialea,b,* 5 6 aDepartment of Microbiology and Immunology, bComprehensive Cancer Center, University of Michigan, 7 Ann Arbor, MI, 48109, USA 8 9 10 11 12 13 14 15 16 17 18 * Corresponding author. Department of Microbiology and Immunology, 1150 West Medical Center 19 Drive, 5724 Medical Science II, Ann Arbor, MI 48109-5620, USA. Tel. +1 (734) 763 9162. Fax: +1 (734) 20 764 3562. 21 E-mail addresses: [email protected] (L. Zhao); [email protected] (M.J. Imperiale). 22 23 24 1 bioRxiv preprint doi: https://doi.org/10.1101/157602; this version posted June 29, 2017. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-NC-ND 4.0 International license. 25 Abstract 26 27 BK polyomavirus (BKPyV) is a human pathogen first isolated in 1971. BKPyV infection is ubiquitous in the 28 human population, with over 80% of adults worldwide being seropositive for BKPyV. BKPyV infection is 29 usually asymptomatic; however, BKPyV reactivation in immunosuppressed transplant patients causes 30 two diseases, polyomavirus-associated nephropathy and hemorrhagic cystitis. -
Interactions Between Polyomavirus Large T Antigen and the Viral Replication Origin Dna: How and Why
INTERACTIONS BETWEEN POLYOMAVIRUS LARGE T ANTIGEN AND THE VIRAL REPLICATION ORIGIN DNA: HOW AND WHY by Yu-Cai Peng Department of Microbiology and Immunology McGill University, Montreal April, 1999 A thesis submitted to the Faculty of Craduate Studies and Re3earch in partial fulfullmeat of the requirements of the degree of doctor of philosophy @Yu-Cai Peng, 1999 National Library Biblioth ue nationale 1+1 of Canada du Cana7 a Acquisitions and Acquisitions et Bibliographie Srvices services bibliographiques 395 Wellmgton Street 395, nie Weliingîm Ottawa ON KIA ON4 OrtawaON K1AON4 Canada Canada The author has granted a non- L'auteur a accordé une licence non exclusive Licence ailowing the exclusive permettant à la National Library of Canada to Bibliothèque nationale du Canada de reproduce, loan, distribute or sell reproduire, prêter, distribuer ou copies of this thesis in microform, vendre des copies de cette thèse sous paper or electronic formats. la forme de microfichelfilm, de reproduction sur papier ou sur format électronique. The author retains ownership of the L'auteur conserve la propriété du copyright in this thesis. Neither the droit d'auteur qui protège cette thèse. thesis nor substantial extracts fkom it Ni la thèse ni des extraits substantiels may be printed or othenvise de celle-ci ne doivent être imprimés reproduced without the author's ou autrement reproduits sans son permission. autorisation. TABLE OF CONTENTS Page Tableofcontents................................................... I Abstract .......................................................... VI Resumé........................................................... VI11 Acknowledgements ................................................. X Claim of contribution to kaowledge ................................... XI Listoffigures ...................................................... XllI Guidelines regarding doctoral thesis ................................... XV CHAPTER 1. INTRODUCTION .................................... 1 1. Overview: Life cycle of polyomavirus and simian virus 40 .......... -
Human Merkel Cell Polyomavirus Small T Antigen Is an Oncoprotein
Research article Human Merkel cell polyomavirus small T antigen is an oncoprotein targeting the 4E-BP1 translation regulator Masahiro Shuda, Hyun Jin Kwun, Huichen Feng, Yuan Chang, and Patrick S. Moore Cancer Virology Program, University of Pittsburgh, Pittsburgh, Pennsylvania, USA. Merkel cell polyomavirus (MCV) is the recently discovered cause of most Merkel cell carcinomas (MCCs), an aggressive form of nonmelanoma skin cancer. Although MCV is known to integrate into the tumor cell genome and to undergo mutation, the molecular mechanisms used by this virus to cause cancer are unknown. Here, we show that MCV small T (sT) antigen is expressed in most MCC tumors, where it is required for tumor cell growth. Unlike the closely related SV40 sT, MCV sT transformed rodent fibroblasts to anchorage- and contact-independent growth and promoted serum-free proliferation of human cells. These effects did not involve protein phosphatase 2A (PP2A) inhibition. MCV sT was found to act downstream in the mam- malian target of rapamycin (mTOR) signaling pathway to preserve eukaryotic translation initiation factor 4E–binding protein 1 (4E-BP1) hyperphosphorylation, resulting in dysregulated cap-dependent translation. MCV sT–associated 4E-BP1 serine 65 hyperphosphorylation was resistant to mTOR complex (mTORC1) and mTORC2 inhibitors. Steady-state phosphorylation of other downstream Akt-mTOR targets, including S6K and 4E-BP2, was also increased by MCV sT. Expression of a constitutively active 4E-BP1 that could not be phosphorylated antagonized the cell transformation activity of MCV sT. Taken together, these experiments showed that 4E-BP1 inhibition is required for MCV transformation. Thus, MCV sT is an oncoprotein, and its effects on dysregulated cap-dependent translation have clinical implications for the prevention, diagnosis, and treatment of MCV-related cancers. -
Autophagy, Evs, and Infections: a Perfect Question for a Perfect Time
REVIEW published: 18 October 2018 doi: 10.3389/fcimb.2018.00362 Autophagy, EVs, and Infections: A Perfect Question for a Perfect Time Michelle L. Pleet 1†, Heather Branscome 1†, Catherine DeMarino 1, Daniel O. Pinto 1, Mohammad Asad Zadeh 1, Myosotys Rodriguez 2, Ilker Kudret Sariyer 3, Nazira El-Hage 2 and Fatah Kashanchi 1* 1 Laboratory of Molecular Virology, School of Systems Biology, George Mason University, Manassas, VA, United States, 2 Department of Immunology, Herbert Wertheim College of Medicine, Florida International University, Miami, FL, United States, 3 Department of Neuroscience, Center for Neurovirology, Lewis Katz School of Medicine, Temple University, Philadelphia, PA, United States Autophagy, a highly conserved process, serves to maintain cellular homeostasis in response to an extensive variety of internal and external stimuli. The classic, or canonical, pathway of autophagy involves the coordinated degradation and recycling of intracellular components and pathogenic material. Proper regulation of autophagy is critical to Edited by: maintain cellular health, as alterations in the autophagy pathway have been linked to the Wenjun Liu, Institute of Microbiology (CAS), China progression of a variety of physiological and pathological conditions in humans, namely Reviewed by: in aging and in viral infection. In addition to its canonical role as a degradative pathway, a Maria Teresa Sanchez-Aparicio, more unconventional and non-degradative role for autophagy has emerged as an area of Icahn School of Medicine at Mount Sinai, United States increasing interest. This process, known as secretory autophagy, is gaining widespread Alan G. Goodman, attention as many viruses are believed to use this pathway as a means to release and Washington State University, spread viral particles. -
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Vehicle Data Codes as of 1/26/2010 Press CTRL + F to prompt the search field. VEHICLE DATA CODES TABLE OF CONTENTS 1--LICENSE PLATE TYPE (LIT) FIELD CODES 1.1 LIT FIELD CODES FOR REGULAR PASSENGER AUTOMOBILE PLATES 1.2 LIT FIELD CODES FOR AIRCRAFT 1.3 LIT FIELD CODES FOR ALL-TERRAIN VEHICLES AND SNOWMOBILES 1.4 SPECIAL LICENSE PLATES 1.5 LIT FIELD CODES FOR SPECIAL LICENSE PLATES 2--VEHICLE MAKE (VMA) AND BRAND NAME (BRA) FIELD CODES 2.1 VMA AND BRA FIELD CODES 2.2 VMA, BRA, AND VMO FIELD CODES FOR AUTOMOBILES, LIGHT-DUTY VANS, LIGHT- DUTY TRUCKS, AND PARTS 2.3 VMA AND BRA FIELD CODES FOR CONSTRUCTION EQUIPMENT AND CONSTRUCTION EQUIPMENT PARTS 2.4 VMA AND BRA FIELD CODES FOR FARM AND GARDEN EQUIPMENT AND FARM EQUIPMENT PARTS 2.5 VMA AND BRA FIELD CODES FOR MOTORCYCLES AND MOTORCYCLE PARTS 2.6 VMA AND BRA FIELD CODES FOR SNOWMOBILES AND SNOWMOBILE PARTS 2.7 VMA AND BRA FIELD CODES FOR TRAILERS AND TRAILER PARTS 2.8 VMA AND BRA FIELD CODES FOR TRUCKS AND TRUCK PARTS 2.9 VMA AND BRA FIELD CODES ALPHABETICALLY BY CODE 3--VEHICLE MODEL (VMO) FIELD CODES 3.1 VMO FIELD CODES FOR AUTOMOBILES, LIGHT-DUTY VANS, AND LIGHT-DUTY TRUCKS 3.2 VMO FIELD CODES FOR ASSEMBLED VEHICLES 3.3 VMO FIELD CODES FOR AIRCRAFT 3.4 VMO FIELD CODES FOR ALL-TERRAIN VEHICLES 3.5 VMO FIELD CODES FOR CONSTRUCTION EQUIPMENT 3.6 VMO FIELD CODES FOR DUNE BUGGIES 3.7 VMO FIELD CODES FOR FARM AND GARDEN EQUIPMENT 3.8 VMO FIELD CODES FOR GO-CARTS 3.9 VMO FIELD CODES FOR GOLF CARTS 3.10 VMO FIELD CODES FOR MOTORIZED RIDE-ON TOYS 3.11 VMO FIELD CODES FOR MOTORIZED WHEELCHAIRS 3.12