Implications of the Virus-Encoded Mirna and Host Mirna in The
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Identification and Interaction Analysis of Molecular Markers in Pancreatic
medRxiv preprint doi: https://doi.org/10.1101/2020.12.20.20248601; this version posted December 23, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted medRxiv a license to display the preprint in perpetuity. All rights reserved. No reuse allowed without permission. Identification and Interaction Analysis of Molecular Markers in Pancreatic Ductal Adenocarcinoma by Integrated Bioinformatics Analysis and Molecular Docking Experiments Basavaraj Vastrad1 , Chanabasayya Vastrad *2, Anandkumar Tengli3 1. Department of Biochemistry, Basaveshwar College of Pharmacy, Gadag, Karnataka 582103, India. 2. Biostatistics and Bioinformatics,Chanabasava Nilaya, Bharthinagar, Dharwad, Karanataka 580001, India. 3. Department of Pharmaceutical Chemistry, JSS College of Pharmacy, Mysuru and JSS Academy of Higher Education & Research, Mysuru- 570015, Karnataka, India. * Chanabasayya Vastrad [email protected] Ph: +919480073398 Chanabasava Nilaya, Bharthinagar, Dharwad 580001 , Karanataka, India NOTE: This preprint reports new research that has not been certified by peer review and should not be used to guide clinical practice. medRxiv preprint doi: https://doi.org/10.1101/2020.12.20.20248601; this version posted December 23, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted medRxiv a license to display the preprint in perpetuity. All rights reserved. No reuse allowed without permission. Abstract The current investigation aimed to mine therapeutic molecular targets that play an key part in the advancement of pancreatic ductal adenocarcinoma (PDAC). The expression profiling by high throughput sequencing dataset profile GSE133684 dataset was downloaded from the Gene Expression Omnibus (GEO) database. -
Non-Coding Rnas: Strategy for Viruses' Offensive
non-coding RNA Review Non-Coding RNAs: Strategy for Viruses’ Offensive Alessia Gallo 1,*, Matteo Bulati 1, Vitale Miceli 1 , Nicola Amodio 2 and Pier Giulio Conaldi 1,3 1 Department of Research, IRCCS ISMETT (Istituto Mediterraneo per i Trapianti e Terapie ad alta specializzazione), Via E.Tricomi 5, 90127 Palermo, Italy; [email protected] (M.B.); [email protected] (V.M.); [email protected] (P.G.C.) 2 Department of Experimental and Clinical Medicine, Magna Graecia University of Catanzaro, 88100 Catanzaro, Italy; [email protected] 3 UPMC Italy (University of Pittsburgh Medical Center Italy), Discesa dei Giudici 4, 90133 Palermo, Italy * Correspondence: [email protected]; Tel.: +39-91-21-92-649 Received: 7 August 2020; Accepted: 8 September 2020; Published: 10 September 2020 Abstract: The awareness of viruses as a constant threat for human public health is a matter of fact and in this resides the need of understanding the mechanisms they use to trick the host. Viral non-coding RNAs are gaining much value and interest for the potential impact played in host gene regulation, acting as fine tuners of host cellular defense mechanisms. The implicit importance of v-ncRNAs resides first in the limited genomes size of viruses carrying only strictly necessary genomic sequences. The other crucial and appealing characteristic of v-ncRNAs is the non-immunogenicity, making them the perfect expedient to be used in the never-ending virus-host war. In this review, we wish to examine how DNA and RNA viruses have evolved a common strategy and which the crucial host pathways are targeted through v-ncRNAs in order to grant and facilitate their life cycle. -
Cows Selected for Divergent Mastitis Susceptibility Display a Differential
J. Dairy Sci. 103:6364–6373 https://doi.org/10.3168/jds.2019-17612 © 2020, The Authors. Published by FASS Inc. and Elsevier Inc. on behalf of the American Dairy Science Association®. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/). Cows selected for divergent mastitis susceptibility display a differential liver transcriptome profile after experimental Staphylococcus aureus mammary gland inoculation A. Heimes,1 J. Brodhagen,1 R. Weikard,1 D. Becker,1 M. M. Meyerholz,2,3 W. Petzl,2 H. Zerbe,2 H.-J. Schuberth,3 M. Hoedemaker,4 M. Schmicke,5 S. Engelmann,6,7 and C. Kühn1,8* 1Leibniz Institute for Farm Animal Biology (FBN), Institute of Genome Biology, 18196 Dummerstorf, Germany 2Clinic for Ruminants with Ambulatory and Herd Health Services, Centre for Clinical Veterinary Medicine, Ludwig-Maximilians-University Munich, 85764 Oberschleißheim, Germany 3Immunology Unit, University of Veterinary Medicine Hannover, 30559 Hannover, Germany 4Clinic for Cattle, University of Veterinary Medicine Hannover, 30173 Hannover, Germany 5Faculty of Natural Sciences III, Martin-Luther Universität Halle-Wittenberg, 06120 Halle, Germany 6Technical University Braunschweig, Institute for Microbiology, 38023 Braunschweig, Germany 7Helmholtz Centre for Infection Research, Microbial Proteomics, 38124 Braunschweig, Germany 8Agricultural and Environmental Faculty, University Rostock, 18059 Rostock, Germany ABSTRACT Key words: BTA18, mastitis, somatic cell score, liver transcriptome, RNAseq Infection and inflammation of the mammary gland, and especially prevention of mastitis, are still major challenges for the dairy industry. Different approaches INTRODUCTION have been tried to reduce the incidence of mastitis. Rapid progress in molecular biology and genetics has Genetic selection of cows with lower susceptibility to made it possible to include information on genomic mastitis promises sustainable success in this regard. -
Supplemental Table S1. Primers for Sybrgreen Quantitative RT-PCR Assays
Supplemental Table S1. Primers for SYBRGreen quantitative RT-PCR assays. Gene Accession Primer Sequence Length Start Stop Tm GC% GAPDH NM_002046.3 GAPDH F TCCTGTTCGACAGTCAGCCGCA 22 39 60 60.43 59.09 GAPDH R GCGCCCAATACGACCAAATCCGT 23 150 128 60.12 56.52 Exon junction 131/132 (reverse primer) on template NM_002046.3 DNAH6 NM_001370.1 DNAH6 F GGGCCTGGTGCTGCTTTGATGA 22 4690 4711 59.66 59.09% DNAH6 R TAGAGAGCTTTGCCGCTTTGGCG 23 4797 4775 60.06 56.52% Exon junction 4790/4791 (reverse primer) on template NM_001370.1 DNAH7 NM_018897.2 DNAH7 F TGCTGCATGAGCGGGCGATTA 21 9973 9993 59.25 57.14% DNAH7 R AGGAAGCCATGTACAAAGGTTGGCA 25 10073 10049 58.85 48.00% Exon junction 9989/9990 (forward primer) on template NM_018897.2 DNAI1 NM_012144.2 DNAI1 F AACAGATGTGCCTGCAGCTGGG 22 673 694 59.67 59.09 DNAI1 R TCTCGATCCCGGACAGGGTTGT 22 822 801 59.07 59.09 Exon junction 814/815 (reverse primer) on template NM_012144.2 RPGRIP1L NM_015272.2 RPGRIP1L F TCCCAAGGTTTCACAAGAAGGCAGT 25 3118 3142 58.5 48.00% RPGRIP1L R TGCCAAGCTTTGTTCTGCAAGCTGA 25 3238 3214 60.06 48.00% Exon junction 3124/3125 (forward primer) on template NM_015272.2 Supplemental Table S2. Transcripts that differentiate IPF/UIP from controls at 5%FDR Fold- p-value Change Transcript Gene p-value p-value p-value (IPF/UIP (IPF/UIP Cluster ID RefSeq Symbol gene_assignment (Age) (Gender) (Smoking) vs. C) vs. C) NM_001178008 // CBS // cystathionine-beta- 8070632 NM_001178008 CBS synthase // 21q22.3 // 875 /// NM_0000 0.456642 0.314761 0.418564 4.83E-36 -2.23 NM_003013 // SFRP2 // secreted frizzled- 8103254 NM_003013 -
Investigating Reptin Function in Acute Myeloid Leukaemia
INVESTIGATING REPTIN FUNCTION IN ACUTE MYELOID LEUKAEMIA Elena Armenteros Monterroso Developmental Biology and Cancer Section Institute of Child Health University College London A thesis submitted for the Degree of Doctor of Philosophy 2017 DECLARATION I, Elena Armenteros Monterroso, confirm that the work presented in this thesis is my own. Where information has been derived from other sources, I confirm that this has been indicated in the thesis. Signature …………………………………….. 2 ACKNOWLEDGEMENTS Firstly, I would like to express my sincere gratitude to my principal supervisor, Dr. Owen Williams, for his excellent advice, support and motivation during the past 4 years. I am extremely grateful for his guidance, but also for the freedom he has given me to pursue my own research. I could not have imagined having a better supervisor. I would also like to extend my gratitude to my second supervisor, Dr. Jasper de Boer. His help and advice have been invaluable. But also the fun environment he has provided in the lab, which made it easier to carry on during stressful times. I am also thankful to all the inspirational people working at the Cancer Section, particularly all the members of my lab, for their help and friendship during the past years. My sincere thanks also goes to all the members of the UCL Genomics team for their efficient work and their help with my sequencing experiments. I am also truly thankful to all my friends, both in the UK and in Spain, for providing the enthusiasm and support that I needed during my studies. I would like to specially thank Miriam, Clare and Heike for their friendship and fun times together. -
Engineered Type 1 Regulatory T Cells Designed for Clinical Use Kill Primary
ARTICLE Acute Myeloid Leukemia Engineered type 1 regulatory T cells designed Ferrata Storti Foundation for clinical use kill primary pediatric acute myeloid leukemia cells Brandon Cieniewicz,1* Molly Javier Uyeda,1,2* Ping (Pauline) Chen,1 Ece Canan Sayitoglu,1 Jeffrey Mao-Hwa Liu,1 Grazia Andolfi,3 Katharine Greenthal,1 Alice Bertaina,1,4 Silvia Gregori,3 Rosa Bacchetta,1,4 Norman James Lacayo,1 Alma-Martina Cepika1,4# and Maria Grazia Roncarolo1,2,4# Haematologica 2021 Volume 106(10):2588-2597 1Department of Pediatrics, Division of Stem Cell Transplantation and Regenerative Medicine, Stanford School of Medicine, Stanford, CA, USA; 2Stanford Institute for Stem Cell Biology and Regenerative Medicine, Stanford School of Medicine, Stanford, CA, USA; 3San Raffaele Telethon Institute for Gene Therapy, Milan, Italy and 4Center for Definitive and Curative Medicine, Stanford School of Medicine, Stanford, CA, USA *BC and MJU contributed equally as co-first authors #AMC and MGR contributed equally as co-senior authors ABSTRACT ype 1 regulatory (Tr1) T cells induced by enforced expression of interleukin-10 (LV-10) are being developed as a novel treatment for Tchemotherapy-resistant myeloid leukemias. In vivo, LV-10 cells do not cause graft-versus-host disease while mediating graft-versus-leukemia effect against adult acute myeloid leukemia (AML). Since pediatric AML (pAML) and adult AML are different on a genetic and epigenetic level, we investigate herein whether LV-10 cells also efficiently kill pAML cells. We show that the majority of primary pAML are killed by LV-10 cells, with different levels of sensitivity to killing. Transcriptionally, pAML sensitive to LV-10 killing expressed a myeloid maturation signature. -
1 Novel Expression Signatures Identified by Transcriptional Analysis
ARD Online First, published on October 7, 2009 as 10.1136/ard.2009.108043 Ann Rheum Dis: first published as 10.1136/ard.2009.108043 on 7 October 2009. Downloaded from Novel expression signatures identified by transcriptional analysis of separated leukocyte subsets in SLE and vasculitis 1Paul A Lyons, 1Eoin F McKinney, 1Tim F Rayner, 1Alexander Hatton, 1Hayley B Woffendin, 1Maria Koukoulaki, 2Thomas C Freeman, 1David RW Jayne, 1Afzal N Chaudhry, and 1Kenneth GC Smith. 1Cambridge Institute for Medical Research and Department of Medicine, Addenbrooke’s Hospital, Hills Road, Cambridge, CB2 0XY, UK 2Roslin Institute, University of Edinburgh, Roslin, Midlothian, EH25 9PS, UK Correspondence should be addressed to Dr Paul Lyons or Prof Kenneth Smith, Department of Medicine, Cambridge Institute for Medical Research, Addenbrooke’s Hospital, Hills Road, Cambridge, CB2 0XY, UK. Telephone: +44 1223 762642, Fax: +44 1223 762640, E-mail: [email protected] or [email protected] Key words: Gene expression, autoimmune disease, SLE, vasculitis Word count: 2,906 The Corresponding Author has the right to grant on behalf of all authors and does grant on behalf of all authors, an exclusive licence (or non-exclusive for government employees) on a worldwide basis to the BMJ Publishing Group Ltd and its Licensees to permit this article (if accepted) to be published in Annals of the Rheumatic Diseases and any other BMJPGL products to exploit all subsidiary rights, as set out in their licence (http://ard.bmj.com/ifora/licence.pdf). http://ard.bmj.com/ on September 29, 2021 by guest. Protected copyright. 1 Copyright Article author (or their employer) 2009. -
Emerging Roles for Natural Microrna Sponges
Emerging Roles for Natural MicroRNA Sponges The MIT Faculty has made this article openly available. Please share how this access benefits you. Your story matters. Citation Ebert, Margaret S., and Phillip A. Sharp. “Emerging Roles for Natural MicroRNA Sponges.” Current Biology 20, no. 19 (October 2010): R858–R861. © 2010 Elsevier. As Published http://dx.doi.org/10.1016/j.cub.2010.08.052 Publisher Elsevier B.V. Version Final published version Citable link http://hdl.handle.net/1721.1/96080 Terms of Use Article is made available in accordance with the publisher's policy and may be subject to US copyright law. Please refer to the publisher's site for terms of use. Current Biology 20, R858–R861, October 12, 2010 ª2010 Elsevier Ltd All rights reserved DOI 10.1016/j.cub.2010.08.052 Emerging Roles for Natural MicroRNA Minireview Sponges Margaret S. Ebert and Phillip A. Sharp miRNAs in a variety of systems: in vitro differentiation of neurons [3] and mesenchymal stem cells [4]; xenografts of cancer cell lines [5,6]; and bone marrow reconstitutions Recently, a non-coding RNA expressed from a human from hematopoietic stem/progenitor cells [7–9]. Germline pseudogene was reported to regulate the corresponding transgenic fruitflies have been shown to generate hypomor- protein-coding mRNA by acting as a decoy for microRNAs phic miRNA phenotypes when sponge expression is induced (miRNAs) that bind to common sites in the 30 untranslated in a tissue-specific manner via the Gal4–UAS system [10]. regions (UTRs). It was proposed that competing for miRNAs might be a general activity of pseudogenes. -
A Tale of Two Rnas During Viral Infection: How Viruses Antagonize Mrnas and Small Non-Coding Rnas in the Host Cell
viruses Review A Tale of Two RNAs during Viral Infection: How Viruses Antagonize mRNAs and Small Non-Coding RNAs in The Host Cell Kristina M. Herbert 1,* and Anita Nag 2,* 1 Department of Experimental Microbiology, Center for Scientific Research and Higher Education of Ensenada (CICESE), Ensenada, Baja California 22860, Mexico 2 Department of Chemistry, Florida A&M University, Tallahassee, FL 32307, USA * Correspondence: [email protected] (K.M.H.); [email protected] (A.N.); Tel.: +52-646-175-0500 (K.M.H.); +1-850-399-5658 (A.N.) Academic Editor: Alexander Ploss Received: 29 March 2016; Accepted: 20 May 2016; Published: 2 June 2016 Abstract: Viral infection initiates an array of changes in host gene expression. Many viruses dampen host protein expression and attempt to evade the host anti-viral defense machinery. Host gene expression is suppressed at several stages of host messenger RNA (mRNA) formation including selective degradation of translationally competent messenger RNAs. Besides mRNAs, host cells also express a variety of noncoding RNAs, including small RNAs, that may also be subject to inhibition upon viral infection. In this review we focused on different ways viruses antagonize coding and noncoding RNAs in the host cell to its advantage. Keywords: mRNA; endonuclease; host shut-off; virus; RNAi 1. Introduction Viral infection has significant effects on the host’s gene expression program. Upon viral infection, mammalian cells activate specific gene expression pathways as a defense response. To assure survival, viruses manipulate the host’s gene expression response pattern in order to maximize viral replication and/or to evade detection by, and block the, host immune responses. -
Murine Cytomegalovirus Encodes a Mir-27 Inhibitor Disguised As a Target
Murine cytomegalovirus encodes a miR-27 inhibitor disguised as a target Valentina Libria,1, Aleksandra Helwakb,1, Pascal Miesenc, Diwakar Santhakumara,d, Jessica G. Borger a, Grzegorz Kudlab, Finn Greye, David Tollerveyb, and Amy H. Bucka,d,2 aCentre for Immunity, Infection and Evolution, University of Edinburgh, Edinburgh EH9 3JT, United Kingdom; bWellcome Trust Centre for Cell Biology, University of Edinburgh, Edinburgh EH9 3JR, United Kingdom; cDepartment of Medical Microbiology, Nijmegen Centre for Molecular Life Sciences, Radboud University Nijmegen Medical Centre, 6500 HB, Nijmegen, The Netherlands; dDivision of Pathway Medicine, University of Edinburgh, Edinburgh EH16 4SB, United Kingdom; and eThe Roslin Institute and Royal (Dick) School of Veterinary Studies, University of Edinburgh, Easter Bush, Midlothian EH25 9RG, United Kingdom Edited* by Norman R. Pace, University of Colorado, Boulder, CO, and approved November 29, 2011 (received for review September 1, 2011) Individual microRNAs (miRNAs) are rapidly down-regulated during involved (16). A small nuclear RNA (snRNA) in Herpesvirus conditions of cellular activation and infection, but factors mediat- saimiri (HVS), HSUR-1, was recently shown to bind to miR-27 ing miRNA turnover are poorly understood. Infection of mouse and mediate its degradation (17). However, no homolog of cells with murine cytomegalovirus (MCMV) induces the rapid HSUR-1 has been identified in other viral families. miRNA down-regulation of an antiviral cellular miRNA, miR-27. Here, we turnover mechanisms in animals remain poorly characterized identify a transcript produced by MCMV that binds to miR-27 and (18). The aim of this work was to identify miR-27 interaction sites mediates its degradation. -
SF3B1-Mutated Chronic Lymphocytic Leukemia Shows Evidence Of
SF3B1-mutated chronic lymphocytic leukemia shows evidence of NOTCH1 pathway activation including CD20 downregulation by Federico Pozzo, Tamara Bittolo, Erika Tissino, Filippo Vit, Elena Vendramini, Luca Laurenti, Giovanni D'Arena, Jacopo Olivieri, Gabriele Pozzato, Francesco Zaja, Annalisa Chiarenza, Francesco Di Raimondo, Antonella Zucchetto, Riccardo Bomben, Francesca Maria Rossi, Giovanni Del Poeta, Michele Dal Bo, and Valter Gattei Haematologica 2020 [Epub ahead of print] Citation: Federico Pozzo, Tamara Bittolo, Erika Tissino, Filippo Vit, Elena Vendramini, Luca Laurenti, Giovanni D'Arena, Jacopo Olivieri, Gabriele Pozzato, Francesco Zaja, Annalisa Chiarenza, Francesco Di Raimondo, Antonella Zucchetto, Riccardo Bomben, Francesca Maria Rossi, Giovanni Del Poeta, Michele Dal Bo, and Valter Gattei SF3B1-mutated chronic lymphocytic leukemia shows evidence of NOTCH1 pathway activation including CD20 downregulation. Haematologica. 2020; 105:xxx doi:10.3324/haematol.2020.261891 Publisher's Disclaimer. E-publishing ahead of print is increasingly important for the rapid dissemination of science. Haematologica is, therefore, E-publishing PDF files of an early version of manuscripts that have completed a regular peer review and have been accepted for publication. E-publishing of this PDF file has been approved by the authors. After having E-published Ahead of Print, manuscripts will then undergo technical and English editing, typesetting, proof correction and be presented for the authors' final approval; the final version of the manuscript will -
Viral Noncoding Rnas: More Surprises
Downloaded from genesdev.cshlp.org on September 24, 2021 - Published by Cold Spring Harbor Laboratory Press REVIEW Viral noncoding RNAs: more surprises Kazimierz T. Tycowski, Yang Eric Guo, Nara Lee, Walter N. Moss, Tenaya K. Vallery, Mingyi Xie, and Joan A. Steitz Department of Molecular Biophysics and Biochemistry, Howard Hughes Medical Institute, Boyer Center for Molecular Medicine, Yale University School of Medicine, New Haven, Connecticut 06536, USA Eukaryotic cells produce several classes of long and small • As for all investigations of viral infection, studying viral noncoding RNA (ncRNA). Many DNA and RNA viruses ncRNAs has richly enhanced our understanding of their synthesize their own ncRNAs. Like their host counter- host cells. In particular, surprising insights into the evo- parts, viral ncRNAs associate with proteins that are essen- lutionary relationships between viruses and their hosts tial for their stability, function, or both. Diverse biological have emerged. With increasing frequency, studies of vi- roles—including the regulation of viral replication, viral ral ncRNAs have led to novel insights into host cell persistence, host immune evasion, and cellular transfor- functioning. — mation have been ascribed to viral ncRNAs. In this re- • In some cases, synthesizing a ncRNA rather than a view, we focus on the multitude of functions played by protein may be the preferred mode of accomplishing a ncRNAs produced by animal viruses. We also discuss function for a virus. RNAs are less immunogenic and their biogenesis and mechanisms of action. therefore can more easily slip under the radar of the host cell immune system. • All viral ncRNAs—like host ncRNAs—associate with — — Like their host cells, many but not all viruses make proteins that are integral to their function.