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Lactobacillus Acidophilus Nucelic Acid Sequences Encoding Carbohydrate Utilization-Related Proteins and Uses Therefor
(19) & (11) EP 2 407 481 A1 (12) EUROPEAN PATENT APPLICATION (43) Date of publication: (51) Int Cl.: 18.01.2012 Bulletin 2012/03 C07K 14/335 (2006.01) C12N 15/31 (2006.01) C12N 15/54 (2006.01) C12N 9/12 (2006.01) (2006.01) (2006.01) (21) Application number: 11176351.2 C12N 15/74 C12Q 1/37 (22) Date of filing: 08.03.2005 (84) Designated Contracting States: • Russel, Michael W. AT BE BG CH CY CZ DE DK EE ES FI FR GB GR Newburgh, IN 47630 (US) HU IE IS IT LI LT LU MC NL PL PT RO SE SI SK TR • Duong, Tri Raleigh, North Carolina 27606 (US) (30) Priority: 08.03.2004 US 551121 P 07.03.2005 US 74226 (74) Representative: Williams, Aylsa D Young & Co LLP (62) Document number(s) of the earlier application(s) in 120 Holborn accordance with Art. 76 EPC: London EC1N 2DY (GB) 10196268.6 / 2 348 041 05760391.2 / 1 727 826 Remarks: •Thecomplete document including Reference Tables (71) Applicant: North Carolina State University and the Sequence Listing can be downloaded from Raleigh, North Carolina 27606 (US) the EPO website •This application was filed on 02-08-2011 as a (72) Inventors: divisional application to the application mentioned • Klaenhammer, Todd Robert under INID code 62. Raleigh, NC 27606 (US) •Claims filed after the date of filing of the application/ • Altermann, Eric after the date of receipt of the divisional application Apex, NC 27539 (US) (Rule 68(4) EPC). • Barrangou, Rodolphe Madison, WI 53718 (US) (54) Lactobacillus acidophilus nucelic acid sequences encoding carbohydrate utilization-related proteins and uses therefor (57) Carbohydrate utilization-related and multidrug invention also provides vectors containing a nucleic acid transporter nucleic acids and polypeptides, and frag- of the invention and cells into which the vector has been ments and variants therof, are disclosed in the current introduced. -
Metabolism of Levulinate and Conversion to the Drug Of
METABOLISM OF LEVULINATE AND CONVERSION TO THE DRUG OF ABUSE 4-HYDROXYPENTANOATE by STEPHANIE R. HARRIS Submitted in partial fulfillment of the requirements For the Degree of Doctor of Philosophy Thesis Advisor: Henri Brunengraber, M.D., Ph.D. Department of Nutrition CASE WESTERN RESERVE UNIVERSITY August 2011 CASE WESTERN RESERVE UNIVERSITY SCHOOL OF GRADUATE STUDIES We hereby approve the thesis/dissertation of STEPHANIE R. HARRIS candidate for the ________________________________ Doctor of Philosophy degree *. (signed) ________________________________________________ Edith Lerner, PhD (Chair of the committee) ________________________________________________ Henri Brunengraber, MD, PhD ________________________________________________ Colleen Croniger, PhD ________________________________________________ Paul Ernsberger, PhD ________________________________________________ Janos Kerner, PhD ________________________________________________ Michelle Puchowicz, PhD (date) _______________________June 16, 2011 *We also certify that written approval has been obtained for any proprietary material contained therein. ii DEDICATION I dedicate this work to my parents and to my husband, Paul. My parents have provided continuous love, encouragement, and guidance throughout my life. They have taught me to set my goals high. My husband has been a source of strength and inspiration, and his dedication and enthusiastic support have helped me achieve this work. iii TABLE OF CONTENTS Table of Contents………………………………………………………………………... iv List of Tables…………………………………………………………………………....viii -
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. -
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. -
Interfaces with Structure Dynamics of the Workhorses from Cells Revealed Through Cross-Linking Mass Spectrometry (CLMS)
biomolecules Review Interfaces with Structure Dynamics of the Workhorses from Cells Revealed through Cross-Linking Mass Spectrometry (CLMS) Umesh Kalathiya 1,*,† , Monikaben Padariya 1,†, Jakub Faktor 1 , Etienne Coyaud 2, Javier A. Alfaro 1,3, Robin Fahraeus 1, Ted R. Hupp 1,3 and David R. Goodlett 1,4,5,* 1 International Centre for Cancer Vaccine Science, University of Gdansk, ul. Kładki 24, 80-822 Gdansk, Poland; [email protected] (M.P.); [email protected] (J.F.); [email protected] (J.A.A.); [email protected] (R.F.); [email protected] (T.R.H.) 2 Protéomique Réponse Inflammatoire Spectrométrie de Mass—PRISM, Inserm U1192, University Lille, CHU Lille, F-59000 Lille, France; [email protected] 3 Institute of Genetics and Molecular Medicine, University of Edinburgh, Edinburgh, Scotland EH4 2XR, UK 4 Department of Biochemistry & Microbiology, University of Victoria, Victoria, BC V8Z 7X8, Canada 5 Genome BC Proteome Centre, University of Victoria, Victoria, BC V8Z 5N3, Canada * Correspondence: [email protected] (U.K.); [email protected] (D.R.G.) † These authors contributed equally to this work. Abstract: The fundamentals of how protein–protein/RNA/DNA interactions influence the structures and functions of the workhorses from the cells have been well documented in the 20th century. A di- Citation: Kalathiya, U.; Padariya, M.; verse set of methods exist to determine such interactions between different components, particularly, Faktor, J.; Coyaud, E.; Alfaro, J.A.; the mass spectrometry (MS) methods, with its advanced instrumentation, has become a significant Fahraeus, R.; Hupp, T.R.; Goodlett, approach to analyze a diverse range of biomolecules, as well as bring insights to their biomolecular D.R. -
LJMU Research Online
LJMU Research Online Fergani, C, Routly, JE, Jones, DN, Pickavance, LC, Smith, RF and Dobson, H KNDy neurone activation prior to the LH surge of the ewe is disrupted by LPS http://researchonline.ljmu.ac.uk/id/eprint/8794/ Article Citation (please note it is advisable to refer to the publisher’s version if you intend to cite from this work) Fergani, C, Routly, JE, Jones, DN, Pickavance, LC, Smith, RF and Dobson, H (2017) KNDy neurone activation prior to the LH surge of the ewe is disrupted by LPS. Reproduction, 154 (3). pp. 281-292. ISSN 1470-1626 LJMU has developed LJMU Research Online for users to access the research output of the University more effectively. Copyright © and Moral Rights for the papers on this site are retained by the individual authors and/or other copyright owners. Users may download and/or print one copy of any article(s) in LJMU Research Online to facilitate their private study or for non-commercial research. You may not engage in further distribution of the material or use it for any profit-making activities or any commercial gain. The version presented here may differ from the published version or from the version of the record. Please see the repository URL above for details on accessing the published version and note that access may require a subscription. For more information please contact [email protected] http://researchonline.ljmu.ac.uk/ 1 1 KNDy neurone activation prior to the LH surge of the ewe is disrupted by LPS 2 C. Fergania, J.E. -
The Determination of Activated Neurokinin B
Examining High Salt Diet, Puberty, and Interactions of Kisspeptin, Neurokinin B, and the Vasopressin Receptor Department of Zoology and Physiology, University of Wyoming Donal Skinner Dori Pitynski Brooke Fallon Background • Early puberty in females • Copenhagen Puberty Study- 2,095 girls • In 1991, mean age: 10.88 years • In 2006, mean age: 9.86 years • Adverse effects (Aksglaede, Pediatrics, 2009) Innovation (Centers for Disease Control and Prevention, 2009) KNDy cells, GnRH, and the reproductive axis • Kisspeptin, Neurokinin B, Dynorphin • GnRH: Gonadotropin releasing hormone (preoptic area) OVERVIEW Specific Aim of Research: 1. Do NKB/Kiss neurons have vasopressin receptors in rat brains? 2. Does salt increase the expression of NKB in rat brains around the time of puberty? Vasopressin • Arcuate nucleus- site of initiation of puberty • Kisspeptin neurons have V1aR- AVPV • Could the same be occurring in arcuate? • Salt = increased release of vasopressin • Link between salt and puberty via kiss/NKB (Shinji, 2013) Methods Brain tissue • Slicing on the cryostat • 20 micron slices • Fixed to slides and labeled for neurotransmitters via immunohistochemistry Immunohistochemistry • Fluorescence, double label (Dr. Mouktahr, Suez Canal University) Primary Antibody Stain 1% Serum Primary Antibody • 48 hours Rinse: 1% PBS + NaN3 Secondary Antibody Stain • Cover-slipped with Vectashield with DAPI Secondary Antibody Results from Kisspeptin/ V1aR double label DAPI V1aR Kisspeptin Merged Neurokinin B/V1aR double label • Antibodies raised in the same -
The Significance of NK1 Receptor Ligands and Their Application In
pharmaceutics Review The Significance of NK1 Receptor Ligands and Their Application in Targeted Radionuclide Tumour Therapy Agnieszka Majkowska-Pilip * , Paweł Krzysztof Halik and Ewa Gniazdowska Centre of Radiochemistry and Nuclear Chemistry, Institute of Nuclear Chemistry and Technology, Dorodna 16, 03-195 Warsaw, Poland * Correspondence: [email protected]; Tel.: +48-22-504-10-11 Received: 7 June 2019; Accepted: 16 August 2019; Published: 1 September 2019 Abstract: To date, our understanding of the Substance P (SP) and neurokinin 1 receptor (NK1R) system shows intricate relations between human physiology and disease occurrence or progression. Within the oncological field, overexpression of NK1R and this SP/NK1R system have been implicated in cancer cell progression and poor overall prognosis. This review focuses on providing an update on the current state of knowledge around the wide spectrum of NK1R ligands and applications of radioligands as radiopharmaceuticals. In this review, data concerning both the chemical and biological aspects of peptide and nonpeptide ligands as agonists or antagonists in classical and nuclear medicine, are presented and discussed. However, the research presented here is primarily focused on NK1R nonpeptide antagonistic ligands and the potential application of SP/NK1R system in targeted radionuclide tumour therapy. Keywords: neurokinin 1 receptor; Substance P; SP analogues; NK1R antagonists; targeted therapy; radioligands; tumour therapy; PET imaging 1. Introduction Neurokinin 1 receptor (NK1R), also known as tachykinin receptor 1 (TACR1), belongs to the tachykinin receptor subfamily of G protein-coupled receptors (GPCRs), also called seven-transmembrane domain receptors (Figure1)[ 1–3]. The human NK1 receptor structure [4] is available in Protein Data Bank (6E59).