SUPPLEMENTAL MATERIAL I. Statistical Analysis Microarray
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Guanine Nucleotidebinding Protein 1 Is One of the Key Molecules
Guanine nucleotide-binding protein 1 is one of the key molecules contributing to cancer cell radioresistance Motoi Fukumoto,1 Tatsuya Amanuma,1 Yoshikazu Kuwahara,1 Tsutomu Shimura,1 Masatoshi Suzuki,1 Shiro Mori,2 Hiroyuki Kumamoto,3 Yohei Saito,4 Yasuhito Ohkubo,4 Zhenfeng Duan,5 Kenji Sano,6 Tomohiro Oguchi,7 Kazuyuki Kainuma,7 Shinichi Usami,7 Kengo Kinoshita,8 Inchul Lee9 and Manabu Fukumoto1 1Department of Pathology, Institute of Development, Aging and Cancer, Tohoku University, Sendai; 2Department of Oral and Maxillofacial Surgery, Tohoku University, Sendai; 3Division of Oral Pathology, Department of Oral Medicine and Surgery, Graduate School of Dentistry, Tohoku University, Sendai; 4Department of Radiopharmacy, Tohoku Pharmaceutical University, Sendai, Japan; 5Department of Hematology/Oncology, Massachusetts General Hospital, Boston, Massachusetts, USA; 6Department of Pathology, School of Medicine, Shinshu University, Matsumoto; 7Department of Otorhinolaryngology, School of Medicine, Shinshu University, Matsumoto, Japan; 8Graduate School of Information Sciences, Tohoku University, Sendai; 9Department of Pathology, Asan Medical Center, Seoul, Korea Key words Standard fractionated radiotherapy for the treatment of cancer consists of daily GTP-binding proteins, head and neck neoplasms, irradiation of 2-Gy X-rays, 5 days a week for 5–8 weeks. To understand the char- neoplasms, radiation, radiation oncology acteristics of radioresistant cancer cells and to develop more effective radiother- Correspondence apy, we established a series of novel, clinically relevant radioresistant (CRR) cells Manabu Fukumoto, Department of Pathology, IDAC, that continue to proliferate with 2-Gy X-ray exposure every 24 h for more than Tohoku University, 4-1 Seiryou-machi, Aoba-ku, Sendai, 30 days in vitro. We studied three human and one murine cell line, and their CRR Japan. -
Genetic Variations in the PSMA6 and PSMC6 Proteasome Genes Are Associated with Multiple Sclerosis and Response to Interferon‑Β Therapy in Latvians
EXPERIMENTAL AND THERAPEUTIC MEDICINE 21: 478, 2021 Genetic variations in the PSMA6 and PSMC6 proteasome genes are associated with multiple sclerosis and response to interferon‑β therapy in Latvians NATALIA PARAMONOVA1, JOLANTA KALNINA1, KRISTINE DOKANE1, KRISTINE DISLERE1, ILVA TRAPINA1, TATJANA SJAKSTE1 and NIKOLAJS SJAKSTE1,2 1Genomics and Bioinformatics, Institute of Biology of The University of Latvia; 2Department of Medical Biochemistry of The University of Latvia, LV‑1004 Riga, Latvia Received July 8, 2020; Accepted December 8, 2020 DOI: 10.3892/etm.2021.9909 Abstract. Several polymorphisms in genes related to the Introduction ubiquitin‑proteasome system exhibit an association with pathogenesis and prognosis of various human autoimmune Multiple sclerosis (MS) is a lifelong demyelinating disease of diseases. Our previous study reported the association the central nervous system. The clinical onset of MS tends to between multiple sclerosis (MS) and the PSMA3‑rs2348071 be between the second and fourth decade of life. Similarly to polymorphism in the Latvian population. The current study other autoimmune diseases, women are affected 3‑4 times more aimed to evaluate the PSMA6 and PSMC6 genetic variations, frequently than men (1). About 10% of MS patients experience their interaction between each other and with the rs2348071, a primary progressive MS form characterized by the progres‑ on the susceptibility to MS risk and response to therapy in sion of neurological disability from the onset. In about 90% the Latvian population. PSMA6‑rs2277460, ‑rs1048990 and of MS patients, the disease undergoes the relapse‑remitting PSMC6‑rs2295826, ‑rs2295827 were genotyped in the MS MS course (RRMS); in most of these patients, the condition case/control study and analysed in terms of genotype‑protein acquires secondary progressive course (SPMS) (2). -
Gene Expression Studies: from Case-Control to Multiple-Population-Based Studies
From the Institute of Human Genetics, Helmholtz Zentrum Munchen,¨ Deutsches Forschungszentrum fur¨ Gesundheit und Umwelt (GmbH) Head: Prof. Dr. Thomas Meitinger Gene expression studies: From case-control to multiple-population-based studies Thesis Submitted for a Doctoral Degree in Natural Sciences at the Faculty of Medicine, Ludwig-Maximilians-Universitat¨ Munchen¨ Katharina Schramm Dachau, Germany 2016 With approval of the Faculty of Medicine Ludwig-Maximilians-Universit¨atM ¨unchen Supervisor/Examiner: Prof. Dr. Thomas Illig Co-Examiners: Prof. Dr. Roland Kappler Dean: Prof. Dr. med. dent. Reinhard Hickel Date of oral examination: 22.12.2016 II Dedicated to my family. III Abstract Recent technological developments allow genome-wide scans of gene expression levels. The reduction of costs and increasing parallelization of processing enable the quantification of 47,000 transcripts in up to twelve samples on a single microarray. Thereby the data collec- tion of large population-based studies was improved. During my PhD, I first developed a workflow for the statistical analyses of case-control stu- dies of up to 50 samples. With large population-based data sets generated I established a pipeline for quality control, data preprocessing and correction for confounders, which re- sulted in substantially improved data. In total, I processed more than 3,000 genome-wide expression profiles using the generated pipeline. With 993 whole blood samples from the population-based KORA (Cooperative Health Research in the Region of Augsburg) study we established one of the largest population-based resource. Using this data set we contributed to a number of transcriptome-wide association studies within national (MetaXpress) and international (CHARGE) consortia. -
A Computational Approach for Defining a Signature of Β-Cell Golgi Stress in Diabetes Mellitus
Page 1 of 781 Diabetes A Computational Approach for Defining a Signature of β-Cell Golgi Stress in Diabetes Mellitus Robert N. Bone1,6,7, Olufunmilola Oyebamiji2, Sayali Talware2, Sharmila Selvaraj2, Preethi Krishnan3,6, Farooq Syed1,6,7, Huanmei Wu2, Carmella Evans-Molina 1,3,4,5,6,7,8* Departments of 1Pediatrics, 3Medicine, 4Anatomy, Cell Biology & Physiology, 5Biochemistry & Molecular Biology, the 6Center for Diabetes & Metabolic Diseases, and the 7Herman B. Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN 46202; 2Department of BioHealth Informatics, Indiana University-Purdue University Indianapolis, Indianapolis, IN, 46202; 8Roudebush VA Medical Center, Indianapolis, IN 46202. *Corresponding Author(s): Carmella Evans-Molina, MD, PhD ([email protected]) Indiana University School of Medicine, 635 Barnhill Drive, MS 2031A, Indianapolis, IN 46202, Telephone: (317) 274-4145, Fax (317) 274-4107 Running Title: Golgi Stress Response in Diabetes Word Count: 4358 Number of Figures: 6 Keywords: Golgi apparatus stress, Islets, β cell, Type 1 diabetes, Type 2 diabetes 1 Diabetes Publish Ahead of Print, published online August 20, 2020 Diabetes Page 2 of 781 ABSTRACT The Golgi apparatus (GA) is an important site of insulin processing and granule maturation, but whether GA organelle dysfunction and GA stress are present in the diabetic β-cell has not been tested. We utilized an informatics-based approach to develop a transcriptional signature of β-cell GA stress using existing RNA sequencing and microarray datasets generated using human islets from donors with diabetes and islets where type 1(T1D) and type 2 diabetes (T2D) had been modeled ex vivo. To narrow our results to GA-specific genes, we applied a filter set of 1,030 genes accepted as GA associated. -
Contributes to Cell-Autonomous Immunity Against Toxoplasma Gondii Elizabeth M
Washington University School of Medicine Digital Commons@Becker Open Access Publications 2013 Guanylate-binding protein 1 (Gbp1) contributes to cell-autonomous immunity against Toxoplasma gondii Elizabeth M. Selleck Washington University School of Medicine in St. Louis Sarah J. Fentress Washington University School of Medicine in St. Louis Wandy L. Beatty Washington University School of Medicine in St. Louis Daniel Degrandi Heinrich-Heine-Universitat Dusseldorf Klaus Pfeffer Heinrich-Heine-Universitat Dusseldorf See next page for additional authors Follow this and additional works at: https://digitalcommons.wustl.edu/open_access_pubs Recommended Citation Selleck, Elizabeth M.; Fentress, Sarah J.; Beatty, Wandy L.; Degrandi, Daniel; Pfeffer, Klaus; Virgin, Herbert W. IV; MacMicking, John D.; and Sibley, L. David, ,"Guanylate-binding protein 1 (Gbp1) contributes to cell-autonomous immunity against Toxoplasma gondii." PLoS Pathogens.,. e1003320. (2013). https://digitalcommons.wustl.edu/open_access_pubs/1496 This Open Access Publication is brought to you for free and open access by Digital Commons@Becker. It has been accepted for inclusion in Open Access Publications by an authorized administrator of Digital Commons@Becker. For more information, please contact [email protected]. Authors Elizabeth M. Selleck, Sarah J. Fentress, Wandy L. Beatty, Daniel Degrandi, Klaus Pfeffer, Herbert W. Virgin IV, John D. MacMicking, and L. David Sibley This open access publication is available at Digital Commons@Becker: https://digitalcommons.wustl.edu/open_access_pubs/1496 Guanylate-binding Protein 1 (Gbp1) Contributes to Cell- autonomous Immunity against Toxoplasma gondii Elizabeth M. Selleck1, Sarah J. Fentress1, Wandy L. Beatty1, Daniel Degrandi2, Klaus Pfeffer2, Herbert W. Virgin IV3, John D. MacMicking4, L. David Sibley1* 1 Department of Molecular Microbiology, Washington University School of Medicine, St. -
Exploring Prostate Cancer Genome Reveals Simultaneous Losses of PTEN, FAS and PAPSS2 in Patients with PSA Recurrence After Radical Prostatectomy
Int. J. Mol. Sci. 2015, 16, 3856-3869; doi:10.3390/ijms16023856 OPEN ACCESS International Journal of Molecular Sciences ISSN 1422-0067 www.mdpi.com/journal/ijms Article Exploring Prostate Cancer Genome Reveals Simultaneous Losses of PTEN, FAS and PAPSS2 in Patients with PSA Recurrence after Radical Prostatectomy Chinyere Ibeawuchi 1, Hartmut Schmidt 2, Reinhard Voss 3, Ulf Titze 4, Mahmoud Abbas 5, Joerg Neumann 6, Elke Eltze 7, Agnes Marije Hoogland 8, Guido Jenster 9, Burkhard Brandt 10 and Axel Semjonow 1,* 1 Prostate Center, Department of Urology, University Hospital Muenster, Albert-Schweitzer-Campus 1, Gebaeude 1A, Muenster D-48149, Germany; E-Mail: [email protected] 2 Center for Laboratory Medicine, University Hospital Muenster, Albert-Schweitzer-Campus 1, Gebaeude 1A, Muenster D-48149, Germany; E-Mail: [email protected] 3 Interdisciplinary Center for Clinical Research, University of Muenster, Albert-Schweitzer-Campus 1, Gebaeude D3, Domagkstrasse 3, Muenster D-48149, Germany; E-Mail: [email protected] 4 Pathology, Lippe Hospital Detmold, Röntgenstrasse 18, Detmold D-32756, Germany; E-Mail: [email protected] 5 Institute of Pathology, Mathias-Spital-Rheine, Frankenburg Street 31, Rheine D-48431, Germany; E-Mail: [email protected] 6 Institute of Pathology, Klinikum Osnabrueck, Am Finkenhuegel 1, Osnabrueck D-49076, Germany; E-Mail: [email protected] 7 Institute of Pathology, Saarbrücken-Rastpfuhl, Rheinstrasse 2, Saarbrücken D-66113, Germany; E-Mail: [email protected] 8 Department -
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PROBING THE INTERACTION OF ASPERGILLUS FUMIGATUS CONIDIA AND HUMAN AIRWAY EPITHELIAL CELLS BY TRANSCRIPTIONAL PROFILING IN BOTH SPECIES by POL GOMEZ B.Sc., The University of British Columbia, 2002 A THESIS SUBMITTED IN PARTIAL FULFILLMENT OF THE REQUIREMENTS FOR THE DEGREE OF MASTER OF SCIENCE in THE FACULTY OF GRADUATE STUDIES (Experimental Medicine) THE UNIVERSITY OF BRITISH COLUMBIA (Vancouver) January 2010 © Pol Gomez, 2010 ABSTRACT The cells of the airway epithelium play critical roles in host defense to inhaled irritants, and in asthma pathogenesis. These cells are constantly exposed to environmental factors, including the conidia of the ubiquitous mould Aspergillus fumigatus, which are small enough to reach the alveoli. A. fumigatus is associated with a spectrum of diseases ranging from asthma and allergic bronchopulmonary aspergillosis to aspergilloma and invasive aspergillosis. Airway epithelial cells have been shown to internalize A. fumigatus conidia in vitro, but the implications of this process for pathogenesis remain unclear. We have developed a cell culture model for this interaction using the human bronchial epithelium cell line 16HBE and a transgenic A. fumigatus strain expressing green fluorescent protein (GFP). Immunofluorescent staining and nystatin protection assays indicated that cells internalized upwards of 50% of bound conidia. Using fluorescence-activated cell sorting (FACS), cells directly interacting with conidia and cells not associated with any conidia were sorted into separate samples, with an overall accuracy of 75%. Genome-wide transcriptional profiling using microarrays revealed significant responses of 16HBE cells and conidia to each other. Significant changes in gene expression were identified between cells and conidia incubated alone versus together, as well as between GFP positive and negative sorted cells. -
Secretion and LPS-Induced Endotoxin Shock Α Lipopolysaccharide
IFIT2 Is an Effector Protein of Type I IFN− Mediated Amplification of Lipopolysaccharide (LPS)-Induced TNF- α Secretion and LPS-Induced Endotoxin Shock This information is current as of September 27, 2021. Alexandra Siegfried, Susanne Berchtold, Birgit Manncke, Eva Deuschle, Julia Reber, Thomas Ott, Michaela Weber, Ulrich Kalinke, Markus J. Hofer, Bastian Hatesuer, Klaus Schughart, Valérie Gailus-Durner, Helmut Fuchs, Martin Hrabe de Angelis, Friedemann Weber, Mathias W. Hornef, Ingo B. Autenrieth and Erwin Bohn Downloaded from J Immunol published online 6 September 2013 http://www.jimmunol.org/content/early/2013/09/06/jimmun ol.1203305 http://www.jimmunol.org/ Supplementary http://www.jimmunol.org/content/suppl/2013/09/06/jimmunol.120330 Material 5.DC1 Why The JI? Submit online. by guest on September 27, 2021 • Rapid Reviews! 30 days* from submission to initial decision • No Triage! Every submission reviewed by practicing scientists • Fast Publication! 4 weeks from acceptance to publication *average Subscription Information about subscribing to The Journal of Immunology is online at: http://jimmunol.org/subscription Permissions Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Email Alerts Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts The Journal of Immunology is published twice each month by The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2013 by The American Association of Immunologists, Inc. All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. Published September 6, 2013, doi:10.4049/jimmunol.1203305 The Journal of Immunology IFIT2 Is an Effector Protein of Type I IFN–Mediated Amplification of Lipopolysaccharide (LPS)-Induced TNF-a Secretion and LPS-Induced Endotoxin Shock Alexandra Siegfried,*,1 Susanne Berchtold,*,1 Birgit Manncke,* Eva Deuschle,* Julia Reber,* Thomas Ott,† Michaela Weber,‡ Ulrich Kalinke,x Markus J. -
Α Are Regulated by Heat Shock Protein 90
The Levels of Retinoic Acid-Inducible Gene I Are Regulated by Heat Shock Protein 90- α Tomoh Matsumiya, Tadaatsu Imaizumi, Hidemi Yoshida, Kei Satoh, Matthew K. Topham and Diana M. Stafforini This information is current as of October 2, 2021. J Immunol 2009; 182:2717-2725; ; doi: 10.4049/jimmunol.0802933 http://www.jimmunol.org/content/182/5/2717 Downloaded from References This article cites 44 articles, 19 of which you can access for free at: http://www.jimmunol.org/content/182/5/2717.full#ref-list-1 Why The JI? Submit online. http://www.jimmunol.org/ • Rapid Reviews! 30 days* from submission to initial decision • No Triage! Every submission reviewed by practicing scientists • Fast Publication! 4 weeks from acceptance to publication *average by guest on October 2, 2021 Subscription Information about subscribing to The Journal of Immunology is online at: http://jimmunol.org/subscription Permissions Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Email Alerts Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts The Journal of Immunology is published twice each month by The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2009 by The American Association of Immunologists, Inc. All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. The Journal of Immunology The Levels of Retinoic Acid-Inducible Gene I Are Regulated by Heat Shock Protein 90-␣1 Tomoh Matsumiya,*‡ Tadaatsu Imaizumi,‡ Hidemi Yoshida,‡ Kei Satoh,‡ Matthew K. Topham,*† and Diana M. Stafforini2*† Retinoic acid-inducible gene I (RIG-I) is an intracellular pattern recognition receptor that plays important roles during innate immune responses to viral dsRNAs. -
Small Nucleolar Rnas Determine Resistance to Doxorubicin in Human Osteosarcoma
International Journal of Molecular Sciences Article Small Nucleolar RNAs Determine Resistance to Doxorubicin in Human Osteosarcoma Martina Godel 1, Deborah Morena 1, Preeta Ananthanarayanan 1, Ilaria Buondonno 1, Giulio Ferrero 2,3 , Claudia M. Hattinger 4, Federica Di Nicolantonio 1,5 , Massimo Serra 4 , 1 2 1, , 1, , Riccardo Taulli , Francesca Cordero , Chiara Riganti * y and Joanna Kopecka * y 1 Department of Oncology, University of Torino, 1026 Torino, Italy; [email protected] (M.G.); [email protected] (D.M.); [email protected] (P.A.); [email protected] (I.B.); [email protected] (F.D.N.); [email protected] (R.T.) 2 Department of Computer Science, University of Torino, 10149 Torino, Italy; [email protected] (G.F.); [email protected] (F.C.) 3 Department of Clinical and Biological Sciences, University of Torino, 10043 Orbassano, Italy 4 Laboratory of Experimental Oncology, Pharmacogenomics and Pharmacogenetics Research Unit, IRCCS Istituto Ortopedico Rizzoli, 40136 Bologna, Italy; [email protected] (C.M.H.); [email protected] (M.S.) 5 Candiolo Cancer Institute, FPO–IRCCS, 10060 Candiolo, Italy * Correspondence: [email protected] (C.R.); [email protected] (J.K.); Tel.: +39-0116705857 (C.R.); +39-0116705849 (J.K.) These authors equally contributed to this work. y Received: 31 May 2020; Accepted: 21 June 2020; Published: 24 June 2020 Abstract: Doxorubicin (Dox) is one of the most important first-line drugs used in osteosarcoma therapy. Multiple and not fully clarified mechanisms, however, determine resistance to Dox. With the aim of identifying new markers associated with Dox-resistance, we found a global up-regulation of small nucleolar RNAs (snoRNAs) in human Dox-resistant osteosarcoma cells. -
Dematin (18): Sc-135881
SAN TA C RUZ BI OTEC HNOL OG Y, INC . Dematin (18): sc-135881 BACKGROUND APPLICATIONS Caldesmon, Filamin 1, Nebulin, Villin, Plastin, ADF, Gelsolin, Dematin and Dematin (18) is recommended for detection of Dematin of mouse, rat and Cofilin are differentially expressed Actin binding proteins. Dematin is a human origin by Western Blotting (starting dilution 1:200, dilution range bundling protein of the erythrocyte membrane skeleton. Dematin is localized 1:100-1:1000), immunoprecipitation [1-2 µg per 100-500 µg of total protein to the spectrin-Actin junctions and its Actin-bundling activity is abolished (1 ml of cell lysate)] and immunofluorescence (starting dilution 1:50, dilution upon phosphorylation by cAMP-dependent protein kinase. It may also play a range 1:50-1:500). role in the regulation of cell shape, implying a role in tumorigenesis. Dematin Suitable for use as control antibody for Dematin siRNA (h): sc-105286, is a trimeric protein containing two identical subunits and a larger subunit. Dematin siRNA (m): sc-142992, Dematin shRNA Plasmid (h): sc-105286-SH, It is localized to the heart, brain, lung, skeletal muscle and kidney. The Dematin shRNA Plasmid (m): sc-142992-SH, Dematin shRNA (h) Lentiviral Dematin gene is located on human chromosome 8p21, a region frequently Particles: sc-105286-V and Dematin shRNA (m) Lentiviral Particles: delet ed in prostate cancer, and mouse chromosome 14. sc-142992-V. REFERENCES Molecular Weight of Dematin: 52/48 kDa. 1. Rana, A.P., et al. 1993. Cloning of human erythroid Dematin reveals Positive Controls: Hep G2 cell lysate: sc-2227. -
Entinostat Augments NK Cell Functions Via Epigenetic Upregulation of IFIT1-STING-STAT4 Pathway
www.oncotarget.com Oncotarget, 2020, Vol. 11, (No. 20), pp: 1799-1815 Research Paper Entinostat augments NK cell functions via epigenetic upregulation of IFIT1-STING-STAT4 pathway John M. Idso1, Shunhua Lao1, Nathan J. Schloemer1,2, Jeffrey Knipstein2, Robert Burns3, Monica S. Thakar1,2,* and Subramaniam Malarkannan1,2,4,5,* 1Laboratory of Molecular Immunology and Immunotherapy, Blood Research Institute, Versiti, Milwaukee, WI, USA 2Division of Pediatric Hematology-Oncology-BMT, Department of Pediatrics, Medical College of Wisconsin, Milwaukee, WI, USA 3Bioinformatics Core, Blood Research Institute, Versiti, Milwaukee, WI, USA 4Divson of Hematology-Oncology, Department of Medicine, Medical College of Wisconsin, Milwaukee, WI, USA 5Department of Microbiology and Immunology, Medical College of Wisconsin, Milwaukee, WI, USA *Co-senior authors Correspondence to: Monica S. Thakar, email: [email protected] Subramaniam Malarkannan, email: [email protected] Keywords: NK cells; histone deacetylase inhibitor; Ewing sarcoma; rhabdomyosarcoma; immunotherapy Received: September 10, 2019 Accepted: March 03, 2020 Published: May 19, 2020 Copyright: Idso et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License 3.0 (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. ABSTRACT Histone deacetylase inhibitors (HDACi) are an emerging cancer therapy; however, their effect on natural killer (NK) cell-mediated anti-tumor responses remain unknown. Here, we evaluated the impact of a benzamide HDACi, entinostat, on human primary NK cells as well as tumor cell lines. Entinostat significantly upregulated the expression of NKG2D, an essential NK cell activating receptor. Independently, entinostat augmented the expression of ULBP1, HLA, and MICA/B on both rhabdomyosarcoma and Ewing sarcoma cell lines.