Viewed in a Table Listing the Recep- Remaining Species-Specific Rhodopsins Are Singles (Shown Tors in the Three Species Studied [See Additional File 1]
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BRIEF COMMUNICATION www.jasn.org Renal Fanconi Syndrome and Hypophosphatemic Rickets in the Absence of Xenotropic and Polytropic Retroviral Receptor in the Nephron Camille Ansermet,* Matthias B. Moor,* Gabriel Centeno,* Muriel Auberson,* † † ‡ Dorothy Zhang Hu, Roland Baron, Svetlana Nikolaeva,* Barbara Haenzi,* | Natalya Katanaeva,* Ivan Gautschi,* Vladimir Katanaev,*§ Samuel Rotman, Robert Koesters,¶ †† Laurent Schild,* Sylvain Pradervand,** Olivier Bonny,* and Dmitri Firsov* BRIEF COMMUNICATION *Department of Pharmacology and Toxicology and **Genomic Technologies Facility, University of Lausanne, Lausanne, Switzerland; †Department of Oral Medicine, Infection, and Immunity, Harvard School of Dental Medicine, Boston, Massachusetts; ‡Institute of Evolutionary Physiology and Biochemistry, St. Petersburg, Russia; §School of Biomedicine, Far Eastern Federal University, Vladivostok, Russia; |Services of Pathology and ††Nephrology, Department of Medicine, University Hospital of Lausanne, Lausanne, Switzerland; and ¶Université Pierre et Marie Curie, Paris, France ABSTRACT Tight control of extracellular and intracellular inorganic phosphate (Pi) levels is crit- leaves.4 Most recently, Legati et al. have ical to most biochemical and physiologic processes. Urinary Pi is freely filtered at the shown an association between genetic kidney glomerulus and is reabsorbed in the renal tubule by the action of the apical polymorphisms in Xpr1 and primary fa- sodium-dependent phosphate transporters, NaPi-IIa/NaPi-IIc/Pit2. However, the milial brain calcification disorder.5 How- molecular identity of the protein(s) participating in the basolateral Pi efflux remains ever, the role of XPR1 in the maintenance unknown. Evidence has suggested that xenotropic and polytropic retroviral recep- of Pi homeostasis remains unknown. Here, tor 1 (XPR1) might be involved in this process. Here, we show that conditional in- we addressed this issue in mice deficient for activation of Xpr1 in the renal tubule in mice resulted in impaired renal Pi Xpr1 in the nephron. -
Dissecting Signaling and Functions of Adhesion G Proteincoupled Receptors
Ann. N.Y. Acad. Sci. ISSN 0077-8923 ANNALS OF THE NEW YORK ACADEMY OF SCIENCES Issue: Annals Meeting Reports Dissecting signaling and functions of adhesion G protein–coupled receptors Demet Arac¸,1 Gabriela Aust,2 Davide Calebiro,3 Felix B. Engel,4 Caroline Formstone,5 Andre´ Goffinet,6 Jorg¨ Hamann,7 Robert J. Kittel,8 Ines Liebscher,9 Hsi-Hsien Lin,10 Kelly R. Monk,11 Alexander Petrenko,12 Xianhua Piao,13 Simone Promel,¨ 9 HelgiB.Schioth,¨ 14 Thue W. Schwartz,15 Martin Stacey,16 Yuri A. Ushkaryov,17 Manja Wobus,18 Uwe Wolfrum,19 Lei Xu,20 and Tobias Langenhan8 1Stanford University, Stanford, California. 2Department of Surgery, Research Laboratories, University of Leipzig, Leipzig, Germany. 3Institute of Pharmacology and Rudolf Virchow Center, DFG-Research Center for Experimental Biomedicine, University of Wurzburg,¨ Wurzburg,¨ Germany. 4Department of Cardiac Development and Remodelling, Max-Planck-Institute for Heart and Lung Research, Bad Nauheim, Germany, and Laboratory of Experimental Renal and Cardiovascular Research, Department of Nephropathology, Institute of Pathology, University of Erlangen-Nurnberg,¨ Erlangen, Germany. 5MRC Centre for Developmental Neurobiology, King’s College London, New Hunts House, London, United Kingdom. 6Universite´ Catholique de Louvain, Institute of Neuroscience, Developmental Neurobiology, Brussels, Belgium. 7Department of Experimental Immunology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands. 8Institute of Physiology, Department of Neurophysiology, University of Wurzburg,¨ Wurzburg,¨ Germany. 9Institute of Biochemistry, Molecular Biochemistry, Medical Faculty, University of Leipzig, Leipzig, Germany. 10Department of Microbiology and Immunology, College of Medicine, Chang Gung University, Tao-Yuan, Taiwan. 11Department of Developmental Biology, Washington University School of Medicine, St. Louis, Missouri. 12Shemyakin-Ovchinnikov Institute of Bioorganic Chemistry, Moscow, Russia. -
Edinburgh Research Explorer
Edinburgh Research Explorer International Union of Basic and Clinical Pharmacology. LXXXVIII. G protein-coupled receptor list Citation for published version: Davenport, AP, Alexander, SPH, Sharman, JL, Pawson, AJ, Benson, HE, Monaghan, AE, Liew, WC, Mpamhanga, CP, Bonner, TI, Neubig, RR, Pin, JP, Spedding, M & Harmar, AJ 2013, 'International Union of Basic and Clinical Pharmacology. LXXXVIII. G protein-coupled receptor list: recommendations for new pairings with cognate ligands', Pharmacological reviews, vol. 65, no. 3, pp. 967-86. https://doi.org/10.1124/pr.112.007179 Digital Object Identifier (DOI): 10.1124/pr.112.007179 Link: Link to publication record in Edinburgh Research Explorer Document Version: Publisher's PDF, also known as Version of record Published In: Pharmacological reviews Publisher Rights Statement: U.S. Government work not protected by U.S. copyright General rights Copyright for the publications made accessible via the Edinburgh Research Explorer is retained by the author(s) and / or other copyright owners and it is a condition of accessing these publications that users recognise and abide by the legal requirements associated with these rights. Take down policy The University of Edinburgh has made every reasonable effort to ensure that Edinburgh Research Explorer content complies with UK legislation. If you believe that the public display of this file breaches copyright please contact [email protected] providing details, and we will remove access to the work immediately and investigate your claim. Download date: 02. Oct. 2021 1521-0081/65/3/967–986$25.00 http://dx.doi.org/10.1124/pr.112.007179 PHARMACOLOGICAL REVIEWS Pharmacol Rev 65:967–986, July 2013 U.S. -
High Throughput Circrna Sequencing Analysis Reveals Novel Insights Into
Xiong et al. Cell Death and Disease (2019) 10:658 https://doi.org/10.1038/s41419-019-1890-9 Cell Death & Disease ARTICLE Open Access High throughput circRNA sequencing analysis reveals novel insights into the mechanism of nitidine chloride against hepatocellular carcinoma Dan-dan Xiong1, Zhen-bo Feng1, Ze-feng Lai2,YueQin2, Li-min Liu3,Hao-xuanFu2, Rong-quan He4,Hua-yuWu5, Yi-wu Dang1, Gang Chen 1 and Dian-zhong Luo1 Abstract Nitidine chloride (NC) has been demonstrated to have an anticancer effect in hepatocellular carcinoma (HCC). However, the mechanism of action of NC against HCC remains largely unclear. In this study, three pairs of NC-treated and NC-untreated HCC xenograft tumour tissues were collected for circRNA sequencing analysis. In total, 297 circRNAs were differently expressed between the two groups, with 188 upregulated and 109 downregulated, among which hsa_circ_0088364 and hsa_circ_0090049 were validated by real-time quantitative polymerase chain reaction. The in vitro experiments showed that the two circRNAs inhibited the malignant biological behaviour of HCC, suggesting that they may play important roles in the development of HCC. To elucidate whether the two circRNAs function as “miRNA sponges” in HCC, we identified circRNA-miRNA and miRNA-mRNA interactions by using the CircInteractome and miRwalk, respectively. Subsequently, 857 miRNA-associated differently expressed genes in HCC were selected for weighted gene co-expression network analysis. Module Eigengene turquoise with 423 genes was found to be significantly related to the survival time, pathology grade and TNM stage of HCC patients. Gene functional enrichment 1234567890():,; 1234567890():,; 1234567890():,; 1234567890():,; analysis showed that the 423 genes mainly functioned in DNA replication- and cell cycle-related biological processes and signalling cascades. -
Supplementary Data
Supplemental Data A novel mouse model of X-linked nephrogenic diabetes insipidus: Phenotypic analysis and therapeutic implications Jian Hua Li, Chung-Lin Chou, Bo Li, Oksana Gavrilova, Christoph Eisner, Jürgen Schnermann, Stasia A. Anderson, Chu-Xia Deng, Mark A. Knepper, and Jürgen Wess Supplemental Methods Metabolic cage studies. Animals were maintained in mouse metabolic cages (Hatteras Instruments, Cary, NC) under controlled temperature and light conditions (12 hr light and dark cycles). Mice received a fixed daily ration of 6.5 g of gelled diet per 20 g of body weight per day. The gelled diet was composed of 4 g of Basal Diet 5755 (Test Diet, Richmond, IN), 2.5 ml of deionized water, and 65 mg agar. Preweighted drinking water was provided ad libitum during the course of the study. Mice were acclimated in the metabolic cages for 1-2 days. Urine was collected under mineral oil in preweighted collection vials for successive 24 hr periods. Analysis of GPCR expression in mouse IMCD cells via TaqMan real-time qRT-PCR. Total RNA prepared from mouse IMCD tubule suspensions was reverse transcribed as described under Experimental Procedures. Tissues from ten 10-week old C57BL/6 WT mice were collected and pooled for each individual experiment. cDNA derived from 640 ng of RNA was mixed with an equal volume of TaqMan gene expression 2 x master mix (Applied Biosystems, Foster City, CA). 100 μl-aliquots of this mixture (corresponding to 80 ng of RNA) were added to each of the 8 fill ports of a 384-well plate of a mouse GPCR array panel (Applied Biosystems). -
Lgr5 Homologues Associate with Wnt Receptors and Mediate R-Spondin Signalling
ARTICLE doi:10.1038/nature10337 Lgr5 homologues associate with Wnt receptors and mediate R-spondin signalling Wim de Lau1*, Nick Barker1{*, Teck Y. Low2, Bon-Kyoung Koo1, Vivian S. W. Li1, Hans Teunissen1, Pekka Kujala3, Andrea Haegebarth1{, Peter J. Peters3, Marc van de Wetering1, Daniel E. Stange1, Johan E. van Es1, Daniele Guardavaccaro1, Richard B. M. Schasfoort4, Yasuaki Mohri5, Katsuhiko Nishimori5, Shabaz Mohammed2, Albert J. R. Heck2 & Hans Clevers1 The adult stem cell marker Lgr5 and its relative Lgr4 are often co-expressed in Wnt-driven proliferative compartments. We find that conditional deletion of both genes in the mouse gut impairs Wnt target gene expression and results in the rapid demise of intestinal crypts, thus phenocopying Wnt pathway inhibition. Mass spectrometry demonstrates that Lgr4 and Lgr5 associate with the Frizzled/Lrp Wnt receptor complex. Each of the four R-spondins, secreted Wnt pathway agonists, can bind to Lgr4, -5 and -6. In HEK293 cells, RSPO1 enhances canonical WNT signals initiated by WNT3A. Removal of LGR4 does not affect WNT3A signalling, but abrogates the RSPO1-mediated signal enhancement, a phenomenon rescued by re-expression of LGR4, -5 or -6. Genetic deletion of Lgr4/5 in mouse intestinal crypt cultures phenocopies withdrawal of Rspo1 and can be rescued by Wnt pathway activation. Lgr5 homologues are facultative Wnt receptor components that mediate Wnt signal enhancement by soluble R-spondin proteins. These results will guide future studies towards the application of R-spondins for regenerative purposes of tissues expressing Lgr5 homologues. The genes Lgr4, Lgr5 and Lgr6 encode orphan 7-transmembrane 4–5 post-induction onwards. -
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. -
Profiling G Protein-Coupled Receptors of Fasciola Hepatica Identifies Orphan Rhodopsins Unique to Phylum Platyhelminthes
bioRxiv preprint doi: https://doi.org/10.1101/207316; this version posted October 23, 2017. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-NC-ND 4.0 International license. 1 Profiling G protein-coupled receptors of Fasciola hepatica 2 identifies orphan rhodopsins unique to phylum 3 Platyhelminthes 4 5 Short title: Profiling G protein-coupled receptors (GPCRs) in Fasciola hepatica 6 7 Paul McVeigh1*, Erin McCammick1, Paul McCusker1, Duncan Wells1, Jane 8 Hodgkinson2, Steve Paterson3, Angela Mousley1, Nikki J. Marks1, Aaron G. Maule1 9 10 11 1Parasitology & Pathogen Biology, The Institute for Global Food Security, School of 12 Biological Sciences, Queen’s University Belfast, Medical Biology Centre, 97 Lisburn 13 Road, Belfast, BT9 7BL, UK 14 15 2 Institute of Infection and Global Health, University of Liverpool, Liverpool, UK 16 17 3 Institute of Integrative Biology, University of Liverpool, Liverpool, UK 18 19 * Corresponding author 20 Email: [email protected] 21 1 bioRxiv preprint doi: https://doi.org/10.1101/207316; this version posted October 23, 2017. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-NC-ND 4.0 International license. 22 Abstract 23 G protein-coupled receptors (GPCRs) are established drug targets. Despite their 24 considerable appeal as targets for next-generation anthelmintics, poor understanding 25 of their diversity and function in parasitic helminths has thwarted progress towards 26 GPCR-targeted anti-parasite drugs. -
Monitoring Nociception by Analyzing Gene Expression Changes in the Central Nervous System of Mice
Zurich Open Repository and Archive University of Zurich Main Library Strickhofstrasse 39 CH-8057 Zurich www.zora.uzh.ch Year: 2010 Monitoring nociception by analyzing gene expression changes in the central nervous system of mice Asner, I N Posted at the Zurich Open Repository and Archive, University of Zurich ZORA URL: https://doi.org/10.5167/uzh-46678 Dissertation Originally published at: Asner, I N. Monitoring nociception by analyzing gene expression changes in the central nervous system of mice. 2010, University of Zurich, Vetsuisse Faculty. Monitoring Nociception by Analyzing Gene Expression Changes in the Central Nervous System of Mice Dissertation zur Erlangung der naturwissenschaftlichen Doktorwürde (Dr. sc. nat) vorgelegt der Mathematisch-naturwissenschaftlichen Fakultät der Universität Zürich von Igor Asner von St. Cergue VD Promotionskomitee Prof. Dr. Peter Sonderegger Prof. Dr. Kurt Bürki Prof. Dr. Hanns Ulrich Zeilhofer Dr. Paolo Cinelli (Leitung der Dissertation) Zürich, 2010 Table of contents Table of content Curriculum vitae 6 Publications 9 Summary 11 Zusammenfassung 14 1. Introduction 17 1.1. Pain and nociception 17 1.1.1 Nociceptive neurons and Mechanoceptors 18 1.1.2 Activation of the nociceptive neurons at the periphery 21 1.1.2.1 Response to noxious heat 22 1.1.2.2 Response to noxious cold 23 1.1.2.3 Response to mechanical stress 24 1.1.3 Nociceptive message processing in the Spinal Cord 25 1.1.3.1 The lamina I and the ascending pathways 25 1.1.3.2 The lamina II and the descending pathways 26 1.1.4 Pain processing and integration in the brain 27 1.1.4.1 The Pain Matrix 27 1.1.4.2 Activation of the descending pathways 29 1.1.5 Inflammatory Pain 31 1.2. -
The Roles Played by Highly Truncated Splice Variants of G Protein-Coupled Receptors Helen Wise
Wise Journal of Molecular Signaling 2012, 7:13 http://www.jmolecularsignaling.com/content/7/1/13 REVIEW Open Access The roles played by highly truncated splice variants of G protein-coupled receptors Helen Wise Abstract Alternative splicing of G protein-coupled receptor (GPCR) genes greatly increases the total number of receptor isoforms which may be expressed in a cell-dependent and time-dependent manner. This increased diversity of cell signaling options caused by the generation of splice variants is further enhanced by receptor dimerization. When alternative splicing generates highly truncated GPCRs with less than seven transmembrane (TM) domains, the predominant effect in vitro is that of a dominant-negative mutation associated with the retention of the wild-type receptor in the endoplasmic reticulum (ER). For constitutively active (agonist-independent) GPCRs, their attenuated expression on the cell surface, and consequent decreased basal activity due to the dominant-negative effect of truncated splice variants, has pathological consequences. Truncated splice variants may conversely offer protection from disease when expression of co-receptors for binding of infectious agents to cells is attenuated due to ER retention of the wild-type co-receptor. In this review, we will see that GPCRs retained in the ER can still be functionally active but also that highly truncated GPCRs may also be functionally active. Although rare, some truncated splice variants still bind ligand and activate cell signaling responses. More importantly, by forming heterodimers with full-length GPCRs, some truncated splice variants also provide opportunities to generate receptor complexes with unique pharmacological properties. So, instead of assuming that highly truncated GPCRs are associated with faulty transcription processes, it is time to reassess their potential benefit to the host organism. -
The Role of the Serotonergic System and the Effects of Antidepressants During Brain Development Examined Using in Vivo Pet Imaging and in Vitro Receptor Binding
From THE DEPARTMENT OF CLINICAL NEUROSCIENCE Karolinska Institutet, Stockholm, Sweden THE ROLE OF THE SEROTONERGIC SYSTEM AND THE EFFECTS OF ANTIDEPRESSANTS DURING BRAIN DEVELOPMENT EXAMINED USING IN VIVO PET IMAGING AND IN VITRO RECEPTOR BINDING Stal Saurav Shrestha Stockholm 2014 Cover Illustration: Voxel-wise analysis of the whole monkey brain using the PET radioligand, [11C]DASB showing persistent serotonin transporter upregulation even after more than 1.5 years of fluoxetine discontinuation. All previously published papers were reproduced with permission from the publisher. Published by Karolinska Institutet. Printed by Universitetsservice-AB © Stal Saurav Shrestha, 2014 ISBN 978-91-7549-522-4 Serotonergic System and Antidepressants During Brain Development To my family Amaze yourself ! Stal Saurav Shrestha, 2014 The Department of Clinical Neuroscience The role of the serotonergic system and the effects of antidepressants during brain development examined using in vivo PET imaging and in vitro receptor binding AKADEMISK AVHANDLING som för avläggande av medicine doktorsexamen vid Karolinska Institutet offentligen försvaras i CMM föreläsningssalen L8:00, Karolinska Universitetssjukhuset, Solna THESIS FOR DOCTORAL DEGREE (PhD) Stal Saurav Shrestha Date: March 31, 2014 (Monday); Time: 10 AM Venue: Center for Molecular Medicine Lecture Hall Floor 1, Karolinska Hospital, Solna Principal Supervisor: Opponent: Robert B. Innis, MD, PhD Klaus-Peter Lesch, MD, PhD National Institutes of Health University of Würzburg Department of NIMH Department -
Molecular Characterization of Clonal Human Renal Forming Cells Cohen-Zontag Osnat , Gershon Rotem , Harari-Steinberg Orit , Kant
bioRxiv preprint doi: https://doi.org/10.1101/2020.03.05.978254; this version posted March 6, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission. Molecular characterization of clonal human renal forming cells Cohen-Zontag Osnat1,7,*, Gershon Rotem1,7,*, Harari-Steinberg Orit1,7,*, Kanter Itamar4, Omer Dorit1,7 , Pleniceanu Oren1,7, Tam Gal4, Oriel Sarit4, Ben-Hur Herzl8,9 , Katz Guy1,3,5,7, Zohar Dotan2,7, Kalisky Tomer4,#, Dekel Benjamin1, 6,7,#,^, Pode- Shakked Naomi1,3,7,#. 1Pediatric Stem Cell Research Institute, Edmond and Lily Safra Children's Hospital, Sheba Medical Center, Tel-Hashomer, Israel 2Dept of Urology, Sheba Medical Center, Tel-Hashomer, Israel 3The Talpiot Medical Leadership Program, Sheba Medical Center, Tel-Hashomer, Israel 4Faculty of Engineering and Bar-Ilan Institute of Nanotechnology and Advanced Materials (BINA), Bar-Ilan University, Ramat Gan, Israel. 5The Joseph Buchman Gynecology and Maternity Center, Sheba Medical Center, Tel- Hashomer, Israel 6Division of Pediatric Nephrology, Edmond and Lily Safra Children's Hospital, Sheba Medical Center, Tel-Hashomer, Israel 7Sackler Faculty of Medicine, Tel-Aviv University, Tel-Aviv, Israel 8L.E.M. Laboratory of Early Detection, Nes Ziona, Israel 9Department of Obstetrics and Gynecology, Assaf Harofeh Medical Center, Tzrifin, Israel *These first authors contributed equally to this work #These senior authors contributed equally to this work ^Correspondence: Benjamin Dekel MD, PhD Pediatric Stem Cell Research Institute Edmond & Lily Safra Children's Hospital, Sheba Medical Center E-mails: [email protected] or [email protected] bioRxiv preprint doi: https://doi.org/10.1101/2020.03.05.978254; this version posted March 6, 2020.