Comparison of Gene Expression Profiles in Chromate Transformed BEAS-2B Cells
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Supplemental Table S1
Entrez Gene Symbol Gene Name Affymetrix EST Glomchip SAGE Stanford Literature HPA confirmed Gene ID Profiling profiling Profiling Profiling array profiling confirmed 1 2 A2M alpha-2-macroglobulin 0 0 0 1 0 2 10347 ABCA7 ATP-binding cassette, sub-family A (ABC1), member 7 1 0 0 0 0 3 10350 ABCA9 ATP-binding cassette, sub-family A (ABC1), member 9 1 0 0 0 0 4 10057 ABCC5 ATP-binding cassette, sub-family C (CFTR/MRP), member 5 1 0 0 0 0 5 10060 ABCC9 ATP-binding cassette, sub-family C (CFTR/MRP), member 9 1 0 0 0 0 6 79575 ABHD8 abhydrolase domain containing 8 1 0 0 0 0 7 51225 ABI3 ABI gene family, member 3 1 0 1 0 0 8 29 ABR active BCR-related gene 1 0 0 0 0 9 25841 ABTB2 ankyrin repeat and BTB (POZ) domain containing 2 1 0 1 0 0 10 30 ACAA1 acetyl-Coenzyme A acyltransferase 1 (peroxisomal 3-oxoacyl-Coenzyme A thiol 0 1 0 0 0 11 43 ACHE acetylcholinesterase (Yt blood group) 1 0 0 0 0 12 58 ACTA1 actin, alpha 1, skeletal muscle 0 1 0 0 0 13 60 ACTB actin, beta 01000 1 14 71 ACTG1 actin, gamma 1 0 1 0 0 0 15 81 ACTN4 actinin, alpha 4 0 0 1 1 1 10700177 16 10096 ACTR3 ARP3 actin-related protein 3 homolog (yeast) 0 1 0 0 0 17 94 ACVRL1 activin A receptor type II-like 1 1 0 1 0 0 18 8038 ADAM12 ADAM metallopeptidase domain 12 (meltrin alpha) 1 0 0 0 0 19 8751 ADAM15 ADAM metallopeptidase domain 15 (metargidin) 1 0 0 0 0 20 8728 ADAM19 ADAM metallopeptidase domain 19 (meltrin beta) 1 0 0 0 0 21 81792 ADAMTS12 ADAM metallopeptidase with thrombospondin type 1 motif, 12 1 0 0 0 0 22 9507 ADAMTS4 ADAM metallopeptidase with thrombospondin type 1 -
Gene Alterations Identified by Expression Profiling in Tumor-Associated Endothelial Cells from Invasive Ovarian Carcinoma
Research Article Gene Alterations Identified by Expression Profiling in Tumor-Associated Endothelial Cells from Invasive Ovarian Carcinoma Chunhua Lu,1 Tomas Bonome,3 Yang Li,1 Aparna A. Kamat,1 Liz Y. Han,1 Rosemarie Schmandt,1 Robert L. Coleman,1 David M. Gershenson,1 Robert B. Jaffe,4 MichaelJ. Birrer, 3 and AnilK. Sood 1,2 Departments of 1Gynecologic Oncology and 2Cancer Biology, University of Texas M. D. Anderson Cancer Center, Houston, Texas; 3Cell and Cancer Biology Branch, National Cancer Institute, Bethesda, Maryland; and 4Center for Reproductive Sciences, University of California, San Francisco, San Francisco, California Abstract the promise of such approaches. However, the full spectrum of Therapeutic strategies based on antiangiogenic approaches differences in the tumor vasculature compared with its normal are beginning to show great promise in clinical studies. counterpart is not known. Identification of additional targets on However, full realization of these approaches requires tumor endothelium may allow opportunities for developing new identification of key differences in gene expression between therapeutic approaches to inhibit angiogenesis in a tumor-specific endothelial cells from tumors versus their normal counter- manner. parts. Here, we examined gene expression differences in Higher levels of proangiogenic cytokines and angiogenesis are purified endothelial cells from 10invasive epithelial ovarian associated with an increased risk of metastasis and poor prognosis cancers and 5 normal ovaries using Affymetrix U133 Plus in ovarian cancer (5, 6). To date, a small number of breast, colon, 2.0microarrays. More than 400differentially expressed genes and brain cancers have been analyzed for gene expression changes were identified in tumor-associated endothelial cells. -
Stroke Genetics and Genomics
Faculdade de Medicina da Universidade de Lisboa Unidade Neurológica de Investigação Clínica PhD Thesis Stroke Genetics and Genomics Tiago Krug Coelho Host Institution: Instituto Gulbenkian de Ciência Supervisor at Instituto Gulbenkian de Ciência: Doctor Sofia Oliveira Supervisor at Faculdade de Medicina da Universidade de Lisboa: Professor José Ferro PhD in Biomedical Sciences Specialization in Neurosciences 2010 Stroke Genetics and Genomics A ciência tem, de facto, um único objectivo: a verdade. Não esgota perfeitamente a sua tarefa se não descobre a causa do todo. Chiara Lubich i Stroke Genetics and Genomics ii Stroke Genetics and Genomics A impressão desta dissertação foi aprovada pela Comissão Coordenadora do Conselho Científico da Faculdade de Medicina de Lisboa em reunião de 28 de Setembro de 2010. iii Stroke Genetics and Genomics iv Stroke Genetics and Genomics As opiniões expressas são da exclusiva responsabilidade do seu autor. v Stroke Genetics and Genomics vi Stroke Genetics and Genomics Abstract ABSTRACT This project presents a comprehensive approach to the identification of new genes that influence the risk for developing stroke. Stroke is the leading cause of death in Portugal and the third leading cause of death in the developed world. It is even more disabling than lethal, and the persistent neurological impairment and physical disability caused by stroke have a very high socioeconomic cost. Moreover, the number of affected individuals is expected to increase with the current aging of the population. Stroke is a “brain attack” cutting off vital blood and oxygen to the brain cells and it is a complex disease resulting from environmental and genetic factors. -
KRAS Mutations Are Negatively Correlated with Immunity in Colon Cancer
www.aging-us.com AGING 2021, Vol. 13, No. 1 Research Paper KRAS mutations are negatively correlated with immunity in colon cancer Xiaorui Fu1,2,*, Xinyi Wang1,2,*, Jinzhong Duanmu1, Taiyuan Li1, Qunguang Jiang1 1Department of Gastrointestinal Surgery, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, People's Republic of China 2Queen Mary College, Medical Department, Nanchang University, Nanchang, Jiangxi, People's Republic of China *Equal contribution Correspondence to: Qunguang Jiang; email: [email protected] Keywords: KRAS mutations, immunity, colon cancer, tumor-infiltrating immune cells, inflammation Received: March 27, 2020 Accepted: October 8, 2020 Published: November 26, 2020 Copyright: © 2020 Fu et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. ABSTRACT The heterogeneity of colon cancer tumors suggests that therapeutics targeting specific molecules may be effective in only a few patients. It is therefore necessary to explore gene mutations in colon cancer. In this study, we obtained colon cancer samples from The Cancer Genome Atlas, and the International Cancer Genome Consortium. We evaluated the landscape of somatic mutations in colon cancer and found that KRAS mutations, particularly rs121913529, were frequent and had prognostic value. Using ESTIMATE analysis, we observed that the KRAS-mutated group had higher tumor purity, lower immune score, and lower stromal score than the wild- type group. Through single-sample Gene Set Enrichment Analysis and Gene Set Enrichment Analysis, we found that KRAS mutations negatively correlated with enrichment levels of tumor infiltrating lymphocytes, inflammation, and cytolytic activities. -
Views for Entrez
BASIC RESEARCH www.jasn.org Phosphoproteomic Analysis Reveals Regulatory Mechanisms at the Kidney Filtration Barrier †‡ †| Markus M. Rinschen,* Xiongwu Wu,§ Tim König, Trairak Pisitkun,¶ Henning Hagmann,* † † † Caroline Pahmeyer,* Tobias Lamkemeyer, Priyanka Kohli,* Nicole Schnell, †‡ †† ‡‡ Bernhard Schermer,* Stuart Dryer,** Bernard R. Brooks,§ Pedro Beltrao, †‡ Marcus Krueger,§§ Paul T. Brinkkoetter,* and Thomas Benzing* *Department of Internal Medicine II, Center for Molecular Medicine, †Cologne Excellence Cluster on Cellular Stress | Responses in Aging-Associated Diseases, ‡Systems Biology of Ageing Cologne, Institute for Genetics, University of Cologne, Cologne, Germany; §Laboratory of Computational Biology, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland; ¶Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand; **Department of Biology and Biochemistry, University of Houston, Houston, Texas; ††Division of Nephrology, Baylor College of Medicine, Houston, Texas; ‡‡European Molecular Biology Laboratory–European Bioinformatics Institute, Hinxton, Cambridge, United Kingdom; and §§Max Planck Institute for Heart and Lung Research, Bad Nauheim, Germany ABSTRACT Diseases of the kidney filtration barrier are a leading cause of ESRD. Most disorders affect the podocytes, polarized cells with a limited capacity for self-renewal that require tightly controlled signaling to maintain their integrity, viability, and function. Here, we provide an atlas of in vivo phosphorylated, glomerulus- expressed -
2017 Bhaloo Shirin Ethesis
This electronic thesis or dissertation has been downloaded from the King’s Research Portal at https://kclpure.kcl.ac.uk/portal/ Vascular Stem Cell Migration in Response to Dkk3 in Vascular Diseases The emergence of a novel chemokine-like protein Bhaloo, Shirin Issa Awarding institution: King's College London The copyright of this thesis rests with the author and no quotation from it or information derived from it may be published without proper acknowledgement. END USER LICENCE AGREEMENT Unless another licence is stated on the immediately following page this work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International licence. https://creativecommons.org/licenses/by-nc-nd/4.0/ You are free to copy, distribute and transmit the work Under the following conditions: Attribution: You must attribute the work in the manner specified by the author (but not in any way that suggests that they endorse you or your use of the work). Non Commercial: You may not use this work for commercial purposes. No Derivative Works - You may not alter, transform, or build upon this work. Any of these conditions can be waived if you receive permission from the author. Your fair dealings and other rights are in no way affected by the above. Take down policy If you believe that this document breaches copyright please contact [email protected] providing details, and we will remove access to the work immediately and investigate your claim. Download date: 09. Oct. 2021 Vascular Stem Cell Migration in Response to Dkk3 in Vascular Diseases The emergence of a novel chemokine-like protein By Shirin Issa Bhaloo A thesis submitted to King’s College London for the degree of Doctor of Philosophy Cardiovascular Division Faculty of Life Sciences & Medicine King’s College London May 2017 0 In dedication to my Family 1 Acknowledgements I wish to express my sincere gratitude to Professor Qingbo Xu for giving me the opportunity to pursue a PhD degree in his laboratory at King’s College London. -
Insights Dust Mite by Influenza a Infection
Downloaded from http://www.jimmunol.org/ by guest on September 29, 2021 is online at: average * The Journal of Immunology , 10 of which you can access for free at: 2012; 188:832-843; Prepublished online 14 from submission to initial decision 4 weeks from acceptance to publication December 2011; doi: 10.4049/jimmunol.1102349 http://www.jimmunol.org/content/188/2/832 Shifting of Immune Responsiveness to House Dust Mite by Influenza A Infection: Genomic Insights Amal Al-Garawi, Mainul Husain, Dora Ilieva, Alison A. Humbles, Roland Kolbeck, Martin R. Stampfli, Paul M. O'Byrne, Anthony J. Coyle and Manel Jordana J Immunol cites 38 articles Submit online. Every submission reviewed by practicing scientists ? is published twice each month by Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts http://jimmunol.org/subscription http://www.jimmunol.org/content/suppl/2011/12/14/jimmunol.110234 9.DC1 This article http://www.jimmunol.org/content/188/2/832.full#ref-list-1 Information about subscribing to The JI No Triage! Fast Publication! Rapid Reviews! 30 days* Why • • • Material References Permissions Email Alerts Subscription Supplementary The Journal of Immunology The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2012 by The American Association of Immunologists, Inc. All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. This information is current as of September 29, 2021. The Journal of Immunology Shifting of Immune Responsiveness to House Dust Mite by Influenza A Infection: Genomic Insights Amal Al-Garawi,*,†,1 Mainul Husain,*,†,1 Dora Ilieva,*,† Alison A. -
1 Imipramine Treatment and Resiliency Exhibit Similar
Imipramine Treatment and Resiliency Exhibit Similar Chromatin Regulation in the Mouse Nucleus Accumbens in Depression Models Wilkinson et al. Supplemental Material 1. Supplemental Methods 2. Supplemental References for Tables 3. Supplemental Tables S1 – S24 SUPPLEMENTAL TABLE S1: Genes Demonstrating Increased Repressive DimethylK9/K27-H3 Methylation in the Social Defeat Model (p<0.001) SUPPLEMENTAL TABLE S2: Genes Demonstrating Decreased Repressive DimethylK9/K27-H3 Methylation in the Social Defeat Model (p<0.001) SUPPLEMENTAL TABLE S3: Genes Demonstrating Increased Repressive DimethylK9/K27-H3 Methylation in the Social Isolation Model (p<0.001) SUPPLEMENTAL TABLE S4: Genes Demonstrating Decreased Repressive DimethylK9/K27-H3 Methylation in the Social Isolation Model (p<0.001) SUPPLEMENTAL TABLE S5: Genes Demonstrating Common Altered Repressive DimethylK9/K27-H3 Methylation in the Social Defeat and Social Isolation Models (p<0.001) SUPPLEMENTAL TABLE S6: Genes Demonstrating Increased Repressive DimethylK9/K27-H3 Methylation in the Social Defeat and Social Isolation Models (p<0.001) SUPPLEMENTAL TABLE S7: Genes Demonstrating Decreased Repressive DimethylK9/K27-H3 Methylation in the Social Defeat and Social Isolation Models (p<0.001) SUPPLEMENTAL TABLE S8: Genes Demonstrating Increased Phospho-CREB Binding in the Social Defeat Model (p<0.001) SUPPLEMENTAL TABLE S9: Genes Demonstrating Decreased Phospho-CREB Binding in the Social Defeat Model (p<0.001) SUPPLEMENTAL TABLE S10: Genes Demonstrating Increased Phospho-CREB Binding in the Social -
(12) United States Patent (10) Patent No.: US 7,615,349 B2 Riker Et Al
US007615349B2 (12) United States Patent (10) Patent No.: US 7,615,349 B2 Riker et al. (45) Date of Patent: Nov. 10, 2009 (54) MELANOMA GENESIGNATURE Barrow et al., “Tumor Antigen Expression in Melanoma Varies According to Antigen and Stage.” Clin. Can. Res., vol. 12:764-771 (75) Inventors: Adam I. Riker, Mobile, AL (US); (2006). Steven Alan Enkemann, Lutz, FL (US) Bauskin et al., “Role of Macrophage Inhibitory Cytokine-1 in Tumorigenesis and Diagnosis of Cancer. Cancer Research, vol. (73) Assignees: H. Lee Moffitt Cancer Center and 66:4983-4986 (2006). Research Institute, Inc., Tampa, FL Baylin et al., “Alterations in DNA Methylation: A Fundamental (US); University of South Florida, Aspect of Neoplasia.” Adv. in Cancer Res, vol. 72: 141-196 (1998). Tampa, FL (US) Bittner et al., “Molecular classification of cutaneous malignant mela noma by gene expression profiling.” Nature, vol. 406:536-540 (*) Notice: Subject to any disclaimer, the term of this (2000). patent is extended or adjusted under 35 Brasseur et al. “Expression of Mage Genes in Primary and Metastatic U.S.C. 154(b) by 0 days. Cutaneous Melanoma.” Int. J. Cancer, vol. 63:375-380 (1995). Cascinelli et al., “Sentinel Lymph Node Biopsy in Cutaneous Mela (21) Appl. No.: 11/852,102 noma: The WHO Melanoma Program Experience.” Annals of Surgi cal Oncology, vol. 7:469-474 (2000). (22) Filed: Sep. 7, 2007 Chen et al., “Decreased PITX1 homeobox gene expression in human lung cancer.” Lung Cancer, vol. 55:287-294 (2007). (65) Prior Publication Data Coppola et al., “Correlation of Osteopontin Protein Expression and US 2008/O113360A1 May 15, 2008 Pathological Stage across a Wide Variety of Tumor Histologies.” Clin. -
Ep 2270226 B1
(19) TZZ Z _T (11) EP 2 270 226 B1 (12) EUROPEAN PATENT SPECIFICATION (45) Date of publication and mention (51) Int Cl.: of the grant of the patent: C12Q 1/68 (2006.01) G01N 33/569 (2006.01) 18.05.2016 Bulletin 2016/20 G01N 33/68 (2006.01) (21) Application number: 10013575.5 (22) Date of filing: 30.03.2006 (54) Method for distinguishing mesenchymal stem cell using molecular marker and use thereof Verfahren zur Unterscheidung mesenchymaler Stammzellen mittels molekularem Marker und Nutzung dieses Marker Procédé de distinction d’une cellule souche mésenchymateuse en utilisant un marqueur moléculaire et son usage (84) Designated Contracting States: (74) Representative: Müller Hoffmann & Partner AT BE BG CH CY CZ DE DK EE ES FI FR GB GR Patentanwälte mbB HU IE IS IT LI LT LU LV MC NL PL PT RO SE SI St.-Martin-Strasse 58 SK TR 81541 München (DE) (30) Priority: 31.03.2005 JP 2005104563 (56) References cited: EP-A1- 1 475 438 WO-A1-02/46373 (43) Date of publication of application: WO-A1-03/016916 WO-A1-03/106492 05.01.2011 Bulletin 2011/01 WO-A2-2004/025293 WO-A2-2004/044142 JP-A- 2004 290 189 US-A1- 2003 161 817 (62) Document number(s) of the earlier application(s) in accordance with Art. 76 EPC: • DESCHASEAUX FREDERIC ET AL: "Direct 06730606.8 / 1 870 455 selection of human bone marrow mesenchymal stem cells using an anti-CD49a antibody reveals (73) Proprietor: Two Cells Co., Ltd their CD45med,low phenotype", BRITISH Minami-ku JOURNAL OF HAEMATOLOGY, Hiroshima City WILEY-BLACKWELL PUBLISHING LTD, GB, vol. -
Pituitary Adenylate Cyclase Activating Polypeptide Signaling Alters Gene Expression in Chick Ciliary Ganglion Neurons
Health Science Campus FINAL APPROVAL OF DISSERTATION Doctor of Philosophy in Biomedical Sciences Pituitary Adenylate Cyclase Activating Polypeptide Signaling Alters Gene Expression In Chick Ciliary Ganglion Neurons Submitted by: Adriane D. Sumner In partial fulfillment of the requirements for the degree of Doctor of Philosophy in Biomedical Sciences Examination Committee Major Advisor: Joseph Margiotta, Ph.D. Academic Linda Dokas, Ph.D. Advisory Committee: David Giovannucci, Ph.D. Marthe Howard, Ph.D. Phyllis Pugh, Ph.D. Senior Associate Dean College of Graduate Studies Michael S. Bisesi, Ph.D. Date of Defense: January 22, 2008 Pituitary Adenylate Cyclase Activating Polypeptide Signaling Alters Gene Expression In Chick Ciliary Ganglion Neurons Adriane D. Sumner University of Toledo College of Medicine 2008 ACKNOWLEDGEMENTS I would like to thank my major advisor, Dr. Joseph Margiotta, and the other members of my advisory committee, Dr. Phyllis Pugh, Dr. Linda Dokas, Dr. Marthe Howard, and Dr. David Giovannucci, for their advice and support during my graduate education. I would like to thank the members of my lab; Dr. Gail Adams, whose help made the microarray experiments possible, Dr. Phyllis Pugh, who designed the primers used in the PAC1 splice variant and VPAC receptor conventional RT-PCR experiments, and Selwyn Jayakar, who has not only been a valuable colleague but a wonderful friend. I am very thankful for the love and support of my family and friends. I am especially grateful to my mom, Pat Sumner, and my sister, Erin Barthel, for all of those long talks and words of encouragement which sustained me through the tough times. I would never have made it without them. -
Dissertation
Dissertation submitted to the Combined Faculties for the Natural Sciences and for Mathematics of the Ruperto-Carola University of Heidelberg, Germany for the degree of Doctor of Natural Sciences presented by Mamatha Sauermann, M.Sc. in Biotechnology Born in Srikakulam, India Date of oral-examination: 27th September, 2006 Development and application of a high throughput cell based assay to identify apoptosis inducing proteins, and functional characterization of the candidate Vacuole Membrane Protein 1 (Vmp1) Referees: PD. Dr. Stefan Wiemann PD. Dr. Frank Breitling To my husband and parents Contents SUMMARY ..................................................................................................................... 1 ZUSAMMENFASSUNG ................................................................................................ 2 1 INTRODUCTION ................................................................................................... 3 1.1 Types of cell death........................................................................................................ 4 1.1.1 Necrosis.................................................................................................................................. 5 1.1.2 Apoptosis ............................................................................................................................... 5 1.2 Organelle specific initiation of apoptosis pathways .................................................. 6 1.2.1 Death Receptor pathway from the plasma membrane (Extrinsic