Supplementary Table 1| the Detailed Clinical Feature of Each Sample Obtained from The
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Supporting Information
Supporting Information Koyanagi et al. 10.1073/pnas.0806215105 SI Materials and Methods CNGB, NM137763; human CNGB1, NM001297; human Amino Acid Sequences. The accession numbers of amino acid CNGB3, NM 019098; box jellyfish CNG, AB435552; fruit fly sequences used for analyses are as follows: Box jellyfish opsin, CNG4, NM 167441; fruit fly CNG3, NM 137871; human AB435549; sea anemone opsin, BR000662; hydra opsin, Con- CNGA4, NM 001037329; fruit fly CNGA, NM 057768; human CNGA1, NM000087; human CNGA2, NM005140; human tig39347:487820–488855 (http://hydrazome.metazome.net); hy- drozaon jellyfish opsin, AB332435; human encephalopsin, CNGA3, NM 001298. AF140242; ragworm c-opsin, AY692353; human rhodopsin, Western Blot Analysis. The proteins extracted from half a rhopalia U49742; human blue, M13299; human red, Z68193; lamprey were separated by 12% SDS/PAGE, transferred onto a PVDF parapinopsin, AB116380; lizard parietopsin, DQ100320; am- membrane, and incubated with 1:500 diluted anti-box jellyfish phioxus peropsin, AB050610; human peropsin, AF012270; hu- opsin antiserum. Visualization was carried out by the ABC man rgr, U15790; squid retinochrome, X57143; human melan- method (Vectastain) and by staining with 3,3Ј-diaminobenzidine opsin, AF147788; amphioxus melanopsin, AB205400; squid (Sigma). rhodopsin, X70498; fruit fly Rh1, K02315; human neuropsin, AY377391; amphioxus rhodopsin, AB050606; scallop Go- In Situ Hybridization. Digoxigenin-labeled antisense and sense RNA rhodopsin, AB006455; human muscarinic acetylcholine receptor probes for the box jellyfish opsin were synthesized by using the DIG M1 (CHRM1), NM000738; human melatonin receptor 1A RNA labeling kit (Roche). Sections were pretreated with protein- (MTNR1A), NM005958; Arabidopsis AKT1, U06745; Arabi- ase K and hybridized with each RNA probe. -
Supporting Information
Supporting Information Celhar et al. 10.1073/pnas.1507052112 SI Materials and Methods using a Nanodrop spectrophotometer (Thermo Fisher Scien- Proteinuria. Proteinuria was assessed using Albustix (Bayer). Al- tific). A TaqMan RNA-to-CT 1-Step Kit (Applied Biosystems) bumin levels in urine were assayed using an Albumin Mouse was used to perform the reverse transcription and quantitative ELISA Kit (Abcam) according to the manufacturer’s instructions; PCR reactions according to the manufacturer’s instructions samples were assayed at a dilution of 1:400. Samples were nor- using TaqMan gene expression assays (Applied Biosystems) to malized for creatinine using a Creatinine (urinary) Colorimetric either Tlr7 (Mm00446590) or the B2m housekeeping gene Assay Kit (Cayman Chemical) according to the manufacturer’s (Mm00437762). Real-time PCR was performed on the 7900H instructions; initial sample dilution of 1:10. fast real-time PCR system and analyzed using SDS 2.4 (Applied Biosystems). Relative mRNA expression was calculated using the Cell Sorting, RNA Isolation, and RT-PCR. Splenic B cells were comparative C method. + − + + t sorted as live CD45 Gr1 B220 CD19 , splenic T cells as live + − + + CD45 Gr1 CD3 CD5 and peritoneal macrophages as live Imaging. Kidney sections from OCT embedded tissue were fixed + − CD45 Gr1 CD11bhiF4/80hi. Sorted cells were centrifuged, re- with 4% paraformaldehyde before permeabilization with acetone suspended in TRIzol (Life Technologies) and stored at −80°. RNA and stained with Phalloidin (AF647) and anti-CD3d (unlabeled was extracted by TRIzol/chloroform and purified with the Qiagen Ab followed by secondary staining with donkey anti-goat Dylight RNeasy Mini purification kit according to the manufacturer’s 550). -
The C9orf72-Interacting Protein Smcr8 Is a Negative Regulator of Autoimmunity and Lysosomal Exocytosis
Downloaded from genesdev.cshlp.org on October 5, 2021 - Published by Cold Spring Harbor Laboratory Press The C9orf72-interacting protein Smcr8 is a negative regulator of autoimmunity and lysosomal exocytosis Yingying Zhang,1,2,3 Aaron Burberry,1,2,3 Jin-Yuan Wang,1,2,3 Jackson Sandoe,1,2,3 Sulagna Ghosh,1,2,3 Namrata D. Udeshi,4 Tanya Svinkina,4 Daniel A. Mordes,1,2,3,5 Joanie Mok,1,2,3 Maura Charlton,1,2,3 Quan-Zhen Li,6,7 Steven A. Carr,4 and Kevin Eggan1,2,3 1Department of Stem Cell and Regenerative Biology, 2Department of Molecular and Cellular Biology, Harvard University, Cambridge, Massachusetts 02138, USA; 3Stanley Center for Psychiatric Research, Broad Institute of Massachusetts Institute of Technology and Harvard, Cambridge, Massachusetts 02142, USA; 4Proteomics Platform, Broad Institute of MIT and Harvard, Cambridge, Massachusetts 02142, USA; 5Department of Pathology, Massachusetts General Hospital, Boston, Massachusetts 02114, USA; 6Department of Immunology, 7Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA While a mutation in C9ORF72 is the most common genetic contributor to amyotrophic lateral sclerosis (ALS), much remains to be learned concerning the function of the protein normally encoded at this locus. To elaborate further on functions for C9ORF72, we used quantitative mass spectrometry-based proteomics to identify interacting proteins in motor neurons and found that its long isoform complexes with and stabilizes SMCR8, which further enables interaction with WDR41. To study the organismal and cellular functions for this tripartite complex, we generated Smcr8 loss-of-function mutant mice and found that they developed phenotypes also observed in C9orf72 loss-of- function animals, including autoimmunity. -
Molecular Mechanisms Involved Involved in the Interaction Effects of HCV and Ethanol on Liver Cirrhosis
Virginia Commonwealth University VCU Scholars Compass Theses and Dissertations Graduate School 2010 Molecular Mechanisms Involved Involved in the Interaction Effects of HCV and Ethanol on Liver Cirrhosis Ryan Fassnacht Virginia Commonwealth University Follow this and additional works at: https://scholarscompass.vcu.edu/etd Part of the Physiology Commons © The Author Downloaded from https://scholarscompass.vcu.edu/etd/2246 This Thesis is brought to you for free and open access by the Graduate School at VCU Scholars Compass. It has been accepted for inclusion in Theses and Dissertations by an authorized administrator of VCU Scholars Compass. For more information, please contact [email protected]. Ryan C. Fassnacht 2010 All Rights Reserved Molecular Mechanisms Involved in the Interaction Effects of HCV and Ethanol on Liver Cirrhosis A thesis submitted in partial fulfillment of the requirements for the degree of Master of Science at Virginia Commonwealth University. by Ryan Christopher Fassnacht, B.S. Hampden Sydney University, 2005 M.S. Virginia Commonwealth University, 2010 Director: Valeria Mas, Ph.D., Associate Professor of Surgery and Pathology Division of Transplant Department of Surgery Virginia Commonwealth University Richmond, Virginia July 9, 2010 Acknowledgement The Author wishes to thank his family and close friends for their support. He would also like to thank the members of the molecular transplant team for their help and advice. This project would not have been possible with out the help of Dr. Valeria Mas and her endearing -
A Functional C-Terminal TRAF3-Binding Site in MAVS Participates in Positive and Negative Regulation of the IFN Antiviral Response
Cell Research (2011) 21:895-910. © 2011 IBCB, SIBS, CAS All rights reserved 1001-0602/11 $ 32.00 npg ORIGINAL ARTICLE www.nature.com/cr A functional C-terminal TRAF3-binding site in MAVS participates in positive and negative regulation of the IFN antiviral response Suzanne Paz1, 2, Myriam Vilasco3, Steven J Werden1, Meztli Arguello1, Deshanthe Joseph-Pillai1, 2, Tiejun Zhao1, Thi Lien-Anh Nguyen1, Qiang Sun1, Eliane F Meurs3, Rongtuan Lin1, 4, John Hiscott1, 2, 4 1Terry Fox Molecular Oncology Group, Lady Davis Institute, Jewish General Hospital, Montreal, Quebec H3T1E2, Canada; 2Department of Microbiology and Immunology, McGill University Montreal, Quebec H3A 2B4, Canada; 3Department of Virology, Unit of Hepacivirus and Innate Immunity, Pasteur Institute, Paris 75724 France; 4Department of Medicine, McGill University Montreal, Quebec H3A 2B4, Canada Recognition of viral RNA structures by the cytosolic sensor retinoic acid-inducible gene-I (RIG-I) results in the activation of signaling cascades that culminate with the generation of the type I interferon (IFN) antiviral response. Onset of antiviral and inflammatory responses to viral pathogens necessitates the regulated spatiotemporal recruitment of signaling adapters, kinases and transcriptional proteins to the mitochondrial antiviral signaling protein (MAVS). We previously demonstrated that the serine/threonine kinase IKKε is recruited to the C-terminal region of MAVS following Sendai or vesicular stomatitis virus (VSV) infection, mediated by Lys63-linked polyubiquitination of MAVS at Lys500, resulting in inhibition of downstream IFN signaling (Paz et al, Mol Cell Biol, 2009). In this study, we demonstrate that C-terminus of MAVS harbors a novel TRAF3-binding site in the aa450- 468 region of MAVS. -
Cytokine Nomenclature
RayBiotech, Inc. The protein array pioneer company Cytokine Nomenclature Cytokine Name Official Full Name Genbank Related Names Symbol 4-1BB TNFRSF Tumor necrosis factor NP_001552 CD137, ILA, 4-1BB ligand receptor 9 receptor superfamily .2. member 9 6Ckine CCL21 6-Cysteine Chemokine NM_002989 Small-inducible cytokine A21, Beta chemokine exodus-2, Secondary lymphoid-tissue chemokine, SLC, SCYA21 ACE ACE Angiotensin-converting NP_000780 CD143, DCP, DCP1 enzyme .1. NP_690043 .1. ACE-2 ACE2 Angiotensin-converting NP_068576 ACE-related carboxypeptidase, enzyme 2 .1 Angiotensin-converting enzyme homolog ACTH ACTH Adrenocorticotropic NP_000930 POMC, Pro-opiomelanocortin, hormone .1. Corticotropin-lipotropin, NPP, NP_001030 Melanotropin gamma, Gamma- 333.1 MSH, Potential peptide, Corticotropin, Melanotropin alpha, Alpha-MSH, Corticotropin-like intermediary peptide, CLIP, Lipotropin beta, Beta-LPH, Lipotropin gamma, Gamma-LPH, Melanotropin beta, Beta-MSH, Beta-endorphin, Met-enkephalin ACTHR ACTHR Adrenocorticotropic NP_000520 Melanocortin receptor 2, MC2-R hormone receptor .1 Activin A INHBA Activin A NM_002192 Activin beta-A chain, Erythroid differentiation protein, EDF, INHBA Activin B INHBB Activin B NM_002193 Inhibin beta B chain, Activin beta-B chain Activin C INHBC Activin C NM005538 Inhibin, beta C Activin RIA ACVR1 Activin receptor type-1 NM_001105 Activin receptor type I, ACTR-I, Serine/threonine-protein kinase receptor R1, SKR1, Activin receptor-like kinase 2, ALK-2, TGF-B superfamily receptor type I, TSR-I, ACVRLK2 Activin RIB ACVR1B -
Overlapping, Additive and Counterregulatory Effects of Type II and I Interferons on Myeloid Dendritic Cell Functions
View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Serveur académique lausannois Review Article TheScientificWorldJOURNAL (2011) 11, 2071–2090 ISSN 1537-744X; doi:10.1100/2011/873895 Overlapping, Additive and Counterregulatory Effects of Type II and I Interferons on Myeloid Dendritic Cell Functions Loredana Frasca and Roberto Lande Department of Infectious, Parasitic and Immune-mediated Diseases, Istituto Superiore di Sanita,` 00161 Rome, Italy Received 8 April 2011; Accepted 27 September 2011 Academic Editor: Fulvio D’Acquisto Dendritic cells (DCs) are central player in immunity by bridging the innate and adaptive arms of the immune system (IS). Interferons (IFNs) are one of the most important factors that regulate both innate and adaptive immunity too. Thus, the understanding of how type II and I IFNs modulate the immune-regulatory properties of DCs is a central issue in immunology. In this paper, we will address this point in the light of the most recent literature, also highlighting the controversial data reported in the field. According to the wide literature available, type II as well as type I IFNs appear, at the same time, to collaborate, to induce additive effects or overlapping functions, as well as to counterregulate each one’s effects on DC biology and, in general, the immune response. The knowledge of these effects has important therapeutic implications in the treatment of infec- tious/autoimmune diseases and cancer and indicates strategies for using IFNs as vaccine adju- vants and in DC-based immune therapeutic approaches. KEYWORDS: IFNs, dendritic cell effector functions, immune activation, immune regulation, cross- regulation Correspondence should be addressed to Loredana Frasca, [email protected] Copyright © 2011 L. -
Expression of Melatonin Receptors 1A/1B, Calmodulin and Estrogen Receptor 2 in Deep Paravertebral Muscles Revisited
MOLECULAR MEDICINE REPORTS 14: 5719-5724, 2016 Etiopathogenesis of adolescent idiopathic scoliosis: Expression of melatonin receptors 1A/1B, calmodulin and estrogen receptor 2 in deep paravertebral muscles revisited JOSEF ZAMECNIK1*, LENKA KRSKOVA1*, JAROMIR HACEK1, IVANA STETKAROVA2 and MARTIN KRBEC3 1Department of Pathology and Molecular Medicine, 2nd Faculty of Medicine, Charles University in Prague and University Hospital Motol, 15006 Prague; 2Department of Neurology, Charles University; 3Department of Orthopedics and Traumatology, 3rd Faculty of Medicine, Charles University in Prague and University Hospital Královské Vinohrady, 10034 Prague, Czech Republic Received October 28, 2015; Accepted October 11, 2016 DOI: 10.3892/mmr.2016.5927 Abstract. The pathogenesis of adolescent idiopathic scoliosis addition, no difference in expression was detected between the (AIS), including the associated local changes in deep para- patients with AIS and the controls. With regards to MTNR1A vertebral muscles, is poorly understood. The asymmetric and MTNR1B, their expression was very weak in paravertebral expression of several molecules involved in the melatonin muscles, and in the majority of cases their expression could signaling pathway, including melatonin receptors 1A/1B not be detected by repeated RT-qPCR analysis. Therefore, (MTNR1A/MTNR1B), estrogen receptor 2 (ESR2) and these data do not support the previously suggested role of the calmodulin (CALM1), has previously been suggested to be asymmetric expression of molecules involved in the melatonin associated with AIS. However, this hypothesis is based on signaling pathway in deep paravertebral muscles in the patho- single studies in which the data were obtained by different genesis of AIS. methodological approaches. Therefore, to evaluate the symmetry of the mRNA expression levels of these molecules, Introduction 18 patients with AIS and 10 non-scoliotic controls were enrolled in the present study. -
Environmental Influences on Endothelial Gene Expression
ENDOTHELIAL CELL GENE EXPRESSION John Matthew Jeff Herbert Supervisors: Prof. Roy Bicknell and Dr. Victoria Heath PhD thesis University of Birmingham August 2012 University of Birmingham Research Archive e-theses repository This unpublished thesis/dissertation is copyright of the author and/or third parties. The intellectual property rights of the author or third parties in respect of this work are as defined by The Copyright Designs and Patents Act 1988 or as modified by any successor legislation. Any use made of information contained in this thesis/dissertation must be in accordance with that legislation and must be properly acknowledged. Further distribution or reproduction in any format is prohibited without the permission of the copyright holder. ABSTRACT Tumour angiogenesis is a vital process in the pathology of tumour development and metastasis. Targeting markers of tumour endothelium provide a means of targeted destruction of a tumours oxygen and nutrient supply via destruction of tumour vasculature, which in turn ultimately leads to beneficial consequences to patients. Although current anti -angiogenic and vascular targeting strategies help patients, more potently in combination with chemo therapy, there is still a need for more tumour endothelial marker discoveries as current treatments have cardiovascular and other side effects. For the first time, the analyses of in-vivo biotinylation of an embryonic system is performed to obtain putative vascular targets. Also for the first time, deep sequencing is applied to freshly isolated tumour and normal endothelial cells from lung, colon and bladder tissues for the identification of pan-vascular-targets. Integration of the proteomic, deep sequencing, public cDNA libraries and microarrays, delivers 5,892 putative vascular targets to the science community. -
Manual Annotation and Analysis of the Defensin Gene Cluster in the C57BL
BMC Genomics BioMed Central Research article Open Access Manual annotation and analysis of the defensin gene cluster in the C57BL/6J mouse reference genome Clara Amid*†1, Linda M Rehaume*†2, Kelly L Brown2,3, James GR Gilbert1, Gordon Dougan1, Robert EW Hancock2 and Jennifer L Harrow1 Address: 1Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridgeshire CB10 1SA, UK, 2University of British Columbia, Centre for Microbial Disease & Immunity Research, 2259 Lower Mall, Vancouver, BC, V6T 1Z4, Canada and 3Department of Rheumatology and Inflammation Research, Göteborg University, Guldhedsgatan 10, S-413 46 Göteborg, Sweden Email: Clara Amid* - [email protected]; Linda M Rehaume* - [email protected]; Kelly L Brown - [email protected]; James GR Gilbert - [email protected]; Gordon Dougan - [email protected]; Robert EW Hancock - [email protected]; Jennifer L Harrow - [email protected] * Corresponding authors †Equal contributors Published: 15 December 2009 Received: 15 May 2009 Accepted: 15 December 2009 BMC Genomics 2009, 10:606 doi:10.1186/1471-2164-10-606 This article is available from: http://www.biomedcentral.com/1471-2164/10/606 © 2009 Amid et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Abstract Background: Host defense peptides are a critical component of the innate immune system. Human alpha- and beta-defensin genes are subject to copy number variation (CNV) and historically the organization of mouse alpha-defensin genes has been poorly defined. -
Mechanism of Action Through an IFN Type I-Independent Responses To
Downloaded from http://www.jimmunol.org/ by guest on September 25, 2021 is online at: average * The Journal of Immunology , 12 of which you can access for free at: 2012; 188:3088-3098; Prepublished online 20 from submission to initial decision 4 weeks from acceptance to publication February 2012; doi: 10.4049/jimmunol.1101764 http://www.jimmunol.org/content/188/7/3088 MF59 and Pam3CSK4 Boost Adaptive Responses to Influenza Subunit Vaccine through an IFN Type I-Independent Mechanism of Action Elena Caproni, Elaine Tritto, Mario Cortese, Alessandro Muzzi, Flaviana Mosca, Elisabetta Monaci, Barbara Baudner, Anja Seubert and Ennio De Gregorio J Immunol cites 33 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/2012/02/21/jimmunol.110176 4.DC1 This article http://www.jimmunol.org/content/188/7/3088.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 -
Genetic and Epigenetic Variation in the Human Genome
Digital Comprehensive Summaries of Uppsala Dissertations from the Faculty of Medicine 122 Genetic and Epigenetic Variation in the Human Genome Analysis of Phenotypically Normal Individuals and Patients Affected with Brain Tumors CECILIA DE BUSTOS ACTA UNIVERSITATIS UPSALIENSIS ISSN 1651-6206 UPPSALA ISBN 91-554-6490-4 2006 urn:nbn:se:uu:diva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