N Small Active Subunit Gene Structure Characterization of Mouse
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Lineage-Specific Evolution of the Vertebrate Otopetrin Gene Family Revealed by Comparative Genomic Analyses
Hurle et al. BMC Evolutionary Biology 2011, 11:23 http://www.biomedcentral.com/1471-2148/11/23 RESEARCHARTICLE Open Access Lineage-specific evolution of the vertebrate Otopetrin gene family revealed by comparative genomic analyses Belen Hurle1, Tomas Marques-Bonet2,3, Francesca Antonacci3, Inna Hughes4, Joseph F Ryan1, NISC Comparative Sequencing Program1,5, Evan E Eichler3, David M Ornitz6, Eric D Green1,5* Abstract Background: Mutations in the Otopetrin 1 gene (Otop1) in mice and fish produce an unusual bilateral vestibular pathology that involves the absence of otoconia without hearing impairment. The encoded protein, Otop1, is the only functionally characterized member of the Otopetrin Domain Protein (ODP) family; the extended sequence and structural preservation of ODP proteins in metazoans suggest a conserved functional role. Here, we use the tools of sequence- and cytogenetic-based comparative genomics to study the Otop1 and the Otop2-Otop3 genes and to establish their genomic context in 25 vertebrates. We extend our evolutionary study to include the gene mutated in Usher syndrome (USH) subtype 1G (Ush1g), both because of the head-to-tail clustering of Ush1g with Otop2 and because Otop1 and Ush1g mutations result in inner ear phenotypes. Results: We established that OTOP1 is the boundary gene of an inversion polymorphism on human chromosome 4p16 that originated in the common human-chimpanzee lineage more than 6 million years ago. Other lineage- specific evolutionary events included a three-fold expansion of the Otop genes in Xenopus tropicalis and of Ush1g in teleostei fish. The tight physical linkage between Otop2 and Ush1g is conserved in all vertebrates. -
Genome Informatics 4–8 September 2002, Wellcome Trust Genome Campus, Hinxton, Cambridge, UK
Comparative and Functional Genomics Comp Funct Genom 2003; 4: 509–514. Published online in Wiley InterScience (www.interscience.wiley.com). DOI: 10.1002/cfg.300 Feature Meeting Highlights: Genome Informatics 4–8 September 2002, Wellcome Trust Genome Campus, Hinxton, Cambridge, UK Jo Wixon1* and Jennifer Ashurst2 1MRC UK HGMP-RC, Hinxton, Cambridge CB10 1SB, UK 2The Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge CB10 1SA, UK *Correspondence to: Abstract Jo Wixon, MRC UK HGMP-RC, Hinxton, Cambridge CB10 We bring you the highlights of the second Joint Cold Spring Harbor Laboratory 1SB, UK. and Wellcome Trust ‘Genome Informatics’ Conference, organized by Ewan Birney, E-mail: [email protected] Suzanna Lewis and Lincoln Stein. There were sessions on in silico data discovery, comparative genomics, annotation pipelines, functional genomics and integrative biology. The conference included a keynote address by Sydney Brenner, who was awarded the 2002 Nobel Prize in Physiology or Medicine (jointly with John Sulston and H. Robert Horvitz) a month later. Copyright 2003 John Wiley & Sons, Ltd. In silico data discovery background set was genes which had a log ratio of ∼0 in liver. Their approach found 17 of 17 known In the first of two sessions on this topic, Naoya promoters with a specificity of 17/28. None of the Hata (Cold Spring Harbor Laboratory, USA) sites they identified was located downstream of a spoke about motif searching for tissue specific TSS and all showed an excess in the foreground promoters. The first step in the process is to sample compared to the background sample. -
The Capacity of Long-Term in Vitro Proliferation of Acute Myeloid
The Capacity of Long-Term in Vitro Proliferation of Acute Myeloid Leukemia Cells Supported Only by Exogenous Cytokines Is Associated with a Patient Subset with Adverse Outcome Annette K. Brenner, Elise Aasebø, Maria Hernandez-Valladares, Frode Selheim, Frode Berven, Ida-Sofie Grønningsæter, Sushma Bartaula-Brevik and Øystein Bruserud Supplementary Material S2 of S31 Table S1. Detailed information about the 68 AML patients included in the study. # of blasts Viability Proliferation Cytokine Viable cells Change in ID Gender Age Etiology FAB Cytogenetics Mutations CD34 Colonies (109/L) (%) 48 h (cpm) secretion (106) 5 weeks phenotype 1 M 42 de novo 241 M2 normal Flt3 pos 31.0 3848 low 0.24 7 yes 2 M 82 MF 12.4 M2 t(9;22) wt pos 81.6 74,686 low 1.43 969 yes 3 F 49 CML/relapse 149 M2 complex n.d. pos 26.2 3472 low 0.08 n.d. no 4 M 33 de novo 62.0 M2 normal wt pos 67.5 6206 low 0.08 6.5 no 5 M 71 relapse 91.0 M4 normal NPM1 pos 63.5 21,331 low 0.17 n.d. yes 6 M 83 de novo 109 M1 n.d. wt pos 19.1 8764 low 1.65 693 no 7 F 77 MDS 26.4 M1 normal wt pos 89.4 53,799 high 3.43 2746 no 8 M 46 de novo 26.9 M1 normal NPM1 n.d. n.d. 3472 low 1.56 n.d. no 9 M 68 MF 50.8 M4 normal D835 pos 69.4 1640 low 0.08 n.d. -
Bioinformatics Analyses of Genomic Imprinting
Bioinformatics Analyses of Genomic Imprinting Dissertation zur Erlangung des Grades des Doktors der Naturwissenschaften der Naturwissenschaftlich-Technischen Fakultät III Chemie, Pharmazie, Bio- und Werkstoffwissenschaften der Universität des Saarlandes von Barbara Hutter Saarbrücken 2009 Tag des Kolloquiums: 08.12.2009 Dekan: Prof. Dr.-Ing. Stefan Diebels Berichterstatter: Prof. Dr. Volkhard Helms Priv.-Doz. Dr. Martina Paulsen Vorsitz: Prof. Dr. Jörn Walter Akad. Mitarbeiter: Dr. Tihamér Geyer Table of contents Summary________________________________________________________________ I Zusammenfassung ________________________________________________________ I Acknowledgements _______________________________________________________II Abbreviations ___________________________________________________________ III Chapter 1 – Introduction __________________________________________________ 1 1.1 Important terms and concepts related to genomic imprinting __________________________ 2 1.2 CpG islands as regulatory elements ______________________________________________ 3 1.3 Differentially methylated regions and imprinting clusters_____________________________ 6 1.4 Reading the imprint __________________________________________________________ 8 1.5 Chromatin marks at imprinted regions___________________________________________ 10 1.6 Roles of repetitive elements ___________________________________________________ 12 1.7 Functional implications of imprinted genes _______________________________________ 14 1.8 Evolution and parental conflict ________________________________________________ -
Toxicogenomics Applications of New Functional Genomics Technologies in Toxicology
\-\w j Toxicogenomics Applications of new functional genomics technologies in toxicology Wilbert H.M. Heijne Proefschrift ter verkrijging vand egraa dva n doctor opgeza gva nd e rector magnificus vanWageninge n Universiteit, Prof.dr.ir. L. Speelman, in netopenbaa r te verdedigen op maandag6 decembe r200 4 des namiddagst e half twee ind eAul a - Table of contents Abstract Chapter I. page 1 General introduction [1] Chapter II page 21 Toxicogenomics of bromobenzene hepatotoxicity: a combined transcriptomics and proteomics approach[2] Chapter III page 48 Bromobenzene-induced hepatotoxicity atth etranscriptom e level PI Chapter IV page 67 Profiles of metabolites and gene expression in rats with chemically induced hepatic necrosis[4] Chapter V page 88 Liver gene expression profiles in relation to subacute toxicity in rats exposed to benzene[5] Chapter VI page 115 Toxicogenomics analysis of liver gene expression in relation to subacute toxicity in rats exposed totrichloroethylen e [6] Chapter VII page 135 Toxicogenomics analysis ofjoin t effects of benzene and trichloroethylene mixtures in rats m Chapter VII page 159 Discussion and conclusions References page 171 Appendices page 187 Samenvatting page 199 Dankwoord About the author Glossary Abbreviations List of genes Chapter I General introduction Parts of this introduction were publishedin : Molecular Biology in Medicinal Chemistry, Heijne etal., 2003 m NATO Advanced Research Workshop proceedings, Heijne eral., 2003 81 Chapter I 1. General introduction 1.1 Background /.1.1 Toxicologicalrisk -
Noelia Díaz Blanco
Effects of environmental factors on the gonadal transcriptome of European sea bass (Dicentrarchus labrax), juvenile growth and sex ratios Noelia Díaz Blanco Ph.D. thesis 2014 Submitted in partial fulfillment of the requirements for the Ph.D. degree from the Universitat Pompeu Fabra (UPF). This work has been carried out at the Group of Biology of Reproduction (GBR), at the Department of Renewable Marine Resources of the Institute of Marine Sciences (ICM-CSIC). Thesis supervisor: Dr. Francesc Piferrer Professor d’Investigació Institut de Ciències del Mar (ICM-CSIC) i ii A mis padres A Xavi iii iv Acknowledgements This thesis has been made possible by the support of many people who in one way or another, many times unknowingly, gave me the strength to overcome this "long and winding road". First of all, I would like to thank my supervisor, Dr. Francesc Piferrer, for his patience, guidance and wise advice throughout all this Ph.D. experience. But above all, for the trust he placed on me almost seven years ago when he offered me the opportunity to be part of his team. Thanks also for teaching me how to question always everything, for sharing with me your enthusiasm for science and for giving me the opportunity of learning from you by participating in many projects, collaborations and scientific meetings. I am also thankful to my colleagues (former and present Group of Biology of Reproduction members) for your support and encouragement throughout this journey. To the “exGBRs”, thanks for helping me with my first steps into this world. Working as an undergrad with you Dr. -
Role of Amylase in Ovarian Cancer Mai Mohamed University of South Florida, [email protected]
University of South Florida Scholar Commons Graduate Theses and Dissertations Graduate School July 2017 Role of Amylase in Ovarian Cancer Mai Mohamed University of South Florida, [email protected] Follow this and additional works at: http://scholarcommons.usf.edu/etd Part of the Pathology Commons Scholar Commons Citation Mohamed, Mai, "Role of Amylase in Ovarian Cancer" (2017). Graduate Theses and Dissertations. http://scholarcommons.usf.edu/etd/6907 This Dissertation is brought to you for free and open access by the Graduate School at Scholar Commons. It has been accepted for inclusion in Graduate Theses and Dissertations by an authorized administrator of Scholar Commons. For more information, please contact [email protected]. Role of Amylase in Ovarian Cancer by Mai Mohamed A dissertation submitted in partial fulfillment of the requirements for the degree of Doctor of Philosophy Department of Pathology and Cell Biology Morsani College of Medicine University of South Florida Major Professor: Patricia Kruk, Ph.D. Paula C. Bickford, Ph.D. Meera Nanjundan, Ph.D. Marzenna Wiranowska, Ph.D. Lauri Wright, Ph.D. Date of Approval: June 29, 2017 Keywords: ovarian cancer, amylase, computational analyses, glycocalyx, cellular invasion Copyright © 2017, Mai Mohamed Dedication This dissertation is dedicated to my parents, Ahmed and Fatma, who have always stressed the importance of education, and, throughout my education, have been my strongest source of encouragement and support. They always believed in me and I am eternally grateful to them. I would also like to thank my brothers, Mohamed and Hussien, and my sister, Mariam. I would also like to thank my husband, Ahmed. -
Relevance Network Between Chemosensitivity and Transcriptome in Human Hepatoma Cells1
Vol. 2, 199–205, February 2003 Molecular Cancer Therapeutics 199 Relevance Network between Chemosensitivity and Transcriptome in Human Hepatoma Cells1 Masaru Moriyama,2 Yujin Hoshida, topoisomerase II  expression, whereas it negatively Motoyuki Otsuka, ShinIchiro Nishimura, Naoya Kato, correlated with expression of carboxypeptidases A3 Tadashi Goto, Hiroyoshi Taniguchi, and Z. Response to nimustine was associated with Yasushi Shiratori, Naohiko Seki, and Masao Omata expression of superoxide dismutase 2. Department of Gastroenterology, Graduate School of Medicine, Relevance networks identified several negative University of Tokyo, Tokyo 113-8655 [M. M., Y. H., M. O., N. K., T. G., H. T., Y. S., M. O.]; Cellular Informatics Team, Computational Biology correlations between gene expression and resistance, Research Center, Tokyo 135-0064 [S. N.]; and Department of which were missed by hierarchical clustering. Our Functional Genomics, Graduate School of Medicine, Chiba University, results suggested the necessity of systematically Chiba 260-8670 [N. S.], Japan evaluating the transporting systems that may play a major role in resistance in hepatoma. This may provide Abstract useful information to modify anticancer drug action in Generally, hepatoma is not a chemosensitive tumor, hepatoma. and the mechanism of resistance to anticancer drugs is not fully elucidated. We aimed to comprehensively Introduction evaluate the relationship between chemosensitivity and Hepatoma is a major cause of death even in developed gene expression profile in human hepatoma cells, by countries, and its incidence is increasing (1). Despite the using microarray analysis, and analyze the data by progress of therapeutic technique (2), the efficacy of radical constructing relevance networks. therapy is hampered by frequent recurrence and advance of In eight hepatoma cell lines (HLE, HLF, Huh7, Hep3B, the tumor (3). -
The New Melanoma: a Novel Model for Disease Progression
DISS. ETH NO. 17606 The new melanoma: A novel model for disease progression A dissertation submitted to SWISS FEDERAL INSTITUTE OF TECHNOLOGY ZÜRICH for the degree of DOCTOR OF SCIENCES presented by Natalie Schlegel Master of Science, Otago University (New Zealand) born on January 20th 1976 citizen of Zürich (ZH) accepted on the recommendation of Professor Sabine Werner, examinor Professor Reinhard Dummer, co-examinor Professor Josef Jiricny, co-examinor 2008 22 Table of Contents Abstract ...................................................................................................................................... 6 Résumé....................................................................................................................................... 8 Abbreviations ........................................................................................................................... 10 1. Introduction ...................................................................................................................... 13 1.1 Definition ................................................................................................................. 14 1.2 Clinical features........................................................................................................ 14 1.3 Pathological features and staging............................................................................. 16 1.3.2 Clark’s level of invasion and Breslow’s thickness........................................... 16 1.3.3 TNM staging ................................................................................................... -
Long Non-Coding RNA Lncshgl Recruits Hnrnpa1 to Suppress Hepatic Gluconeogenesis and Lipogenesis
Page 1 of 60 Diabetes Long non-coding RNA LncSHGL recruits hnRNPA1 to suppress hepatic gluconeogenesis and lipogenesis Junpei Wang1,2#, Weili Yang1,2#, Zhenzhen Chen1, Ji Chen1, Yuhong Meng1, Biaoqi Feng1, Libo Sun3, Lin Dou4, Jian Li4, Qinghua Cui2*, Jichun Yang1* 1Department of Physiology and Pathophysiology, School of Basic Medical Sciences Key Laboratory of Molecular Cardiovascular Sciences of the Ministry of Education Center for Non-coding RNA Medicine Peking University Health Science Center Beijing 100191, China 2Department of Biomedical Informatics, School of Basic Medical Sciences Key Laboratory of Molecular Cardiovascular Sciences of the Ministry of Education, Center for Non-coding RNA Medicine Peking University Health Science Center, Beijing 100191, China 3Beijing You An Hospital,Capital Medical University, Beijing 100069, China 4Key Laboratory of Geriatrics, Beijing Institute of Geriatrics & Beijing Hospital, Ministry of Health, Beijing 100730, China #These authors contributed equally to this work *Correspondence to: Jichun Yang, Ph.D. Department of Physiology and Pathophysiology, School of Basic Medical Sciences Peking University Health Science Center, Beijing 100191, China Email: [email protected]; Tel: (+86) 10-82801403 Or to: Qinghua Cui, Ph.D. Department of Biomedical Informatics, School of Basic Medical Sciences Peking University Health Science Center, Beijing 100191, China Email:[email protected]; Tel:(+86)10-82801585 1 Diabetes Publish Ahead of Print, published online January 30, 2018 Diabetes Page 2 of 60 Abstract Mammalian genomes encode a huge number of LncRNAs with unknown functions. This study determined the role and mechanism of a new LncRNA, LncRNA Suppressor of Hepatic Gluconeogenesis and Lipogenesis (LncSHGL), in regulating hepatic glucose/lipid metabolism. -
Role and Regulation of the P53-Homolog P73 in the Transformation of Normal Human Fibroblasts
Role and regulation of the p53-homolog p73 in the transformation of normal human fibroblasts Dissertation zur Erlangung des naturwissenschaftlichen Doktorgrades der Bayerischen Julius-Maximilians-Universität Würzburg vorgelegt von Lars Hofmann aus Aschaffenburg Würzburg 2007 Eingereicht am Mitglieder der Promotionskommission: Vorsitzender: Prof. Dr. Dr. Martin J. Müller Gutachter: Prof. Dr. Michael P. Schön Gutachter : Prof. Dr. Georg Krohne Tag des Promotionskolloquiums: Doktorurkunde ausgehändigt am Erklärung Hiermit erkläre ich, dass ich die vorliegende Arbeit selbständig angefertigt und keine anderen als die angegebenen Hilfsmittel und Quellen verwendet habe. Diese Arbeit wurde weder in gleicher noch in ähnlicher Form in einem anderen Prüfungsverfahren vorgelegt. Ich habe früher, außer den mit dem Zulassungsgesuch urkundlichen Graden, keine weiteren akademischen Grade erworben und zu erwerben gesucht. Würzburg, Lars Hofmann Content SUMMARY ................................................................................................................ IV ZUSAMMENFASSUNG ............................................................................................. V 1. INTRODUCTION ................................................................................................. 1 1.1. Molecular basics of cancer .......................................................................................... 1 1.2. Early research on tumorigenesis ................................................................................. 3 1.3. Developing -
Suppression of the Peripheral Immune System Limits the Central Immune Response Following Cuprizone-Feeding: Relevance to Modelling Multiple Sclerosis
cells Article Suppression of the Peripheral Immune System Limits the Central Immune Response Following Cuprizone-Feeding: Relevance to Modelling Multiple Sclerosis Monokesh K. Sen 1 , Mohammed S. M. Almuslehi 1,2, Erika Gyengesi 1, Simon J. Myers 3, Peter J. Shortland 3, David A. Mahns 1,* and Jens R. Coorssen 4,* 1 School of Medicine, Western Sydney University, Locked Bag 1797, Penrith, NSW 2751, Australia; [email protected] (M.K.S.); [email protected] (M.S.M.A.); [email protected] (E.G.) 2 Department of Physiology, College of Veterinary Medicine, Diyala University, Diyala, Iraq 3 School of Science and Health, Western Sydney University, Locked Bag 1797, Penrith, NSW 2751, Australia; [email protected] (S.J.M.); [email protected] (P.J.S.) 4 Department of Health Sciences, Faculty of Applied Health Sciences, and Department of Biological Sciences, Faculty of Mathematics and Science, Brock University, St. Catharines, Ontario, ON L2S 3A1, Canada * Correspondence: [email protected] (D.A.M.); [email protected] (J.R.C.); Tel.: +02-4620-3784 (D.A.M.); +905-688-5550 (J.R.C.) Received: 6 September 2019; Accepted: 18 October 2019; Published: 24 October 2019 Abstract: Cuprizone (CPZ) preferentially affects oligodendrocytes (OLG), resulting in demyelination. To investigate whether central oligodendrocytosis and gliosis triggered an adaptive immune response, the impact of combining a standard (0.2%) or low (0.1%) dose of ingested CPZ with disruption of the blood brain barrier (BBB), using pertussis toxin (PT), was assessed in mice. 0.2% CPZ( PT) for ± 5 weeks produced oligodendrocytosis, demyelination and gliosis plus marked splenic atrophy (37%) and reduced levels of CD4 (44%) and CD8 (61%).