Recombinant Human OSCAR Protein Catalog Number: ATGP2129

Total Page：16

File Type：pdf, Size：1020Kb

Recombinant human OSCAR protein Catalog Number: ATGP2129 PRODUCT INPORMATION Expression system E.coli Domain 19-286aa UniProt No. Q8IYS5 NCBI Accession No. NP_996554 Alternative Names Osteoclast-associated immunoglobulin-like receptor isoform 1, PIGR3 PRODUCT SPECIFICATION Molecular Weight 31 kDa (291aa) Concentration 0.25mg/ml (determined by Bradford assay) Formulation Liquid in. 20mM Tris-HCl buffer (pH 8.0) containing 0.4M urea, 10% glycerol Purity > 85% by SDS-PAGE Tag His-Tag Application SDS-PAGE,Denatured Storage Condition Can be stored at +2C to +8C for 1 week. For long term storage, aliquot and store at -20C to -80C. Avoid repeated freezing and thawing cycles. BACKGROUND Description Osteoclasts are multinucleated cells that resorb bone and are essential for bone homeostasis. OSCAR is a member of the leukocyte receptor complex (LRC) protein family that plays critical roles in the regulation of both innate and adaptive immune responses. Different from the other LRC members, OSCAR expression is detected specifically in preosteoclasts or mature osteoclasts. OSCAR may be an important bone-specific regulator of osteoclast differentiation. Multiple alternatively spliced transcript variants encoding different isoforms have been found for this gene. Recombinant human OSCAR protein, fused to His-tag at N-terminus, was expressed in E. coli. 1 Recombinant human OSCAR protein Catalog Number: ATGP2129 Amino acid Sequence MGSSHHHHHH SSGLVPRGSH MGSDITPSVA IIVPPASYHP KPWLGAQPAT VVTPGVNVTL RCRAPQPAWR FGLFKPGEIA PLLFRDVSSE LAEFFLEEVT PAQGGIYRCC YRRPDWGPGV WSQPSDVLEL LVTEELPRPS LVALPGPVVG PGANVSLRCA GRLRNMSFVL YREGVAAPLQ YRHSAQPWAD FTLLGARAPG TYSCYYHTPS APYVLSQRSE VLVISWEGEG PEARPASSAP GMQAPGPPPS DPGAQAPSLS SFRPRGLVLQ PLLPQTQDSW DPAPPPSDPG V General References Kim N, Takami M, et al. (2002). J Exp Med. 195(2):201-9. DATA SDS-PAGE 3ug by SDS-PAGE under reducing condition and visualized by coomassie blue stain. 2.

Copy Link

Recommended publications

Elephantid Genomes Reveal the Molecular Bases of Woolly Mammoth Adaptations to the Arctic
Article Elephantid Genomes Reveal the Molecular Bases of Woolly Mammoth Adaptations to the Arctic Graphical Abstract Authors Vincent J. Lynch, Oscar C. Bedoya-Reina, Aakrosh Ratan, ..., George H. Perry, Webb Miller, Stephan C. Schuster Correspondence [email protected] (V.J.L.), [email protected] (W.M.) In Brief Lynch et al. sequence complete genomes from three Asian elephants and two woolly mammoths and identify amino acid changes unique to woolly mammoths. Woolly-mammoth-specific amino acid changes underlie cold- adapted traits in mammoths, including small ears, thick fur, and altered temperature sensation. Highlights d Complete genomes of three Asian elephants and two woolly mammoths were sequenced d Mammoth-specific amino acid changes were found in 1,642 protein-coding genes d Genes with mammoth-specific changes are associated with adaptation to extreme cold d An amino acid change in TRPV3 may have altered temperature sensation in mammoths Lynch et al., 2015, Cell Reports 12, 217–228 July 14, 2015 ª2015 The Authors http://dx.doi.org/10.1016/j.celrep.2015.06.027 Cell Reports Article Elephantid Genomes Reveal the Molecular Bases of Woolly Mammoth Adaptations to the Arctic Vincent J. Lynch,1,* Oscar C. Bedoya-Reina,2,4 Aakrosh Ratan,2,5 Michael Sulak,1 Daniela I. Drautz-Moses,2,6 George H. Perry,3 Webb Miller,2,* and Stephan C. Schuster2,6 1Department of Human Genetics, The University of Chicago, 920 East 58th Street, CLSC 319C, Chicago, IL 60637, USA 2Center for Comparative Genomics and Bioinformatics, Pennsylvania State University, 506B
[Show full text]
2020 Program Book
PROGRAM BOOK Note that TAGC was cancelled and held online with a different schedule and program. This document serves as a record of the original program designed for the in-person meeting. April 22–26, 2020 Gaylord National Resort & Convention Center Metro Washington, DC TABLE OF CONTENTS About the GSA ........................................................................................................................................................ 3 Conference Organizers ...........................................................................................................................................4 General Information ...............................................................................................................................................7 Mobile App ....................................................................................................................................................7 Registration, Badges, and Pre-ordered T-shirts .............................................................................................7 Oral Presenters: Speaker Ready Room - Camellia 4.......................................................................................7 Poster Sessions and Exhibits - Prince George’s Exhibition Hall ......................................................................7 GSA Central - Booth 520 ................................................................................................................................8 Internet Access ..............................................................................................................................................8
[Show full text]
Functional Analysis of Somatic Mutations Affecting Receptor Tyrosine Kinase Family in Metastatic Colorectal Cancer
Author Manuscript Published OnlineFirst on March 29, 2019; DOI: 10.1158/1535-7163.MCT-18-0582 Author manuscripts have been peer reviewed and accepted for publication but have not yet been edited. Functional analysis of somatic mutations affecting receptor tyrosine kinase family in metastatic colorectal cancer Leslie Duplaquet1, Martin Figeac2, Frédéric Leprêtre2, Charline Frandemiche3,4, Céline Villenet2, Shéhérazade Sebda2, Nasrin Sarafan-Vasseur5, Mélanie Bénozène1, Audrey Vinchent1, Gautier Goormachtigh1, Laurence Wicquart6, Nathalie Rousseau3, Ludivine Beaussire5, Stéphanie Truant7, Pierre Michel8, Jean-Christophe Sabourin9, Françoise Galateau-Sallé10, Marie-Christine Copin1,6, Gérard Zalcman11, Yvan De Launoit1, Véronique Fafeur1 and David Tulasne1 1 Univ. Lille, CNRS, Institut Pasteur de Lille, UMR 8161 - M3T – Mechanisms of Tumorigenesis and Target Therapies, F-59000 Lille, France. 2 Univ. Lille, Plateau de génomique fonctionnelle et structurale, CHU Lille, F-59000 Lille, France 3 TCBN - Tumorothèque Caen Basse-Normandie, F-14000 Caen, France. 4 Réseau Régional de Cancérologie – OncoBasseNormandie – F14000 Caen – France. 5 Normandie Univ, UNIROUEN, Inserm U1245, IRON group, Rouen University Hospital, Normandy Centre for Genomic and Personalized Medicine, F-76000 Rouen, France. 6 Tumorothèque du C2RC de Lille, F-59037 Lille, France. 7 Department of Digestive Surgery and Transplantation, CHU Lille, Univ Lille, 2 Avenue Oscar Lambret, 59037, Lille Cedex, France. 8 Department of hepato-gastroenterology, Rouen University Hospital, Normandie Univ, UNIROUEN, Inserm U1245, IRON group, F-76000 Rouen, France. 9 Department of Pathology, Normandy University, INSERM 1245, Rouen University Hospital, F 76 000 Rouen, France. 10 Department of Pathology, MESOPATH-MESOBANK, Centre León Bérard, Lyon, France. 11 Thoracic Oncology Department, CIC1425/CLIP2 Paris-Nord, Hôpital Bichat-Claude Bernard, Paris, France.
[Show full text]
Signals Through Two Different Pathways Immunoglobulin Receptor Able to Transduce of Cd300b, a New Activating Molecular and Funct
Molecular and Functional Characterization of CD300b, a New Activating Immunoglobulin Receptor Able to Transduce Signals through Two Different Pathways This information is current as of September 26, 2021. Águeda Martínez-Barriocanal and Joan Sayós J Immunol 2006; 177:2819-2830; ; doi: 10.4049/jimmunol.177.5.2819 http://www.jimmunol.org/content/177/5/2819 Downloaded from References This article cites 47 articles, 20 of which you can access for free at: http://www.jimmunol.org/content/177/5/2819.full#ref-list-1 http://www.jimmunol.org/ Why The JI? Submit online. • 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 by guest on September 26, 2021 *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 © 2006 by The American Association of Immunologists All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. The Journal of Immunology Molecular and Functional Characterization of CD300b, a New Activating Immunoglobulin Receptor Able to Transduce Signals through Two Different Pathways1 A´ gueda Martı´nez-Barriocanal and Joan Sayo´s2 In this study, we describe the characterization of human CD300b, a novel member of the CMRF-35/immune receptor expressed by myeloid cell (IREM) multigene family of immune receptors.
[Show full text]
Gene Expression Profiling of Nfatc1-Knockdown In
cells Article Gene Expression Profiling of NFATc1-Knockdown in RAW 264.7 Cells: An Alternative Pathway for Macrophage Differentiation Roberta Russo , Selene Mallia, Francesca Zito and Nadia Lampiasi * Institute of Biomedicine and Molecular Immunology “Alberto Monroy”, National Research Council, Via Ugo La Malfa 153, 90146 Palermo, Italy; [email protected] (R.R.); [email protected] (S.M.); [email protected] (F.Z.) * Correspondence: [email protected]; Tel.: +39-091-680-9513 Received: 13 December 2018; Accepted: 5 February 2019; Published: 7 February 2019 Abstract: NFATc1, which is ubiquitous in many cell types, is the master regulator of osteoclastogenesis. However, the molecular mechanisms by which NFATc1 drives its transcriptional program to produce osteoclasts from macrophages (M) remains poorly understood. We performed quantitative PCR (QPCR) arrays and bioinformatic analyses to discover new direct and indirect NFATc1 targets. The results revealed that NFATc1 significantly modified the expression of 55 genes in untransfected cells and 31 genes after NFATc1-knockdown (≥2). Among them, we focused on 19 common genes that showed changes in the PCR arrays between the two groups of cells. Gene Ontology (GO) demonstrated that genes related to cell differentiation and the development process were significantly (p > 0.05) affected by NFATc1-knockdown. Among all the genes analyzed, we focused on GATA2, which was up-regulated in NFATc1-knockdown cells, while its expression was reduced after NFATc1 rescue. Thus, we suggest GATA2 as a new target of NFATc1. Ingenuity Pathway Analysis (IPA) identified up-regulated GATA2 and the STAT family members as principal nodes involved in cell differentiation.
[Show full text]
Genome Informatics
Joint Cold Spring Harbor Laboratory/Wellcome Trust Conference GENOME INFORMATICS September 15–September 19, 2010 View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Cold Spring Harbor Laboratory Institutional Repository Joint Cold Spring Harbor Laboratory/Wellcome Trust Conference GENOME INFORMATICS September 15–September 19, 2010 Arranged by Inanc Birol, BC Cancer Agency, Canada Michele Clamp, BioTeam, Inc. James Kent, University of California, Santa Cruz, USA SCHEDULE AT A GLANCE Wednesday 15th September 2010 17.00-17.30 Registration – finger buffet dinner served from 17.30-19.30 19.30-20:50 Session 1: Epigenomics and Gene Regulation 20.50-21.10 Break 21.10-22.30 Session 1, continued Thursday 16th September 2010 07.30-09.00 Breakfast 09.00-10.20 Session 2: Population and Statistical Genomics 10.20-10:40 Morning Coffee 10:40-12:00 Session 2, continued 12.00-14.00 Lunch 14.00-15.20 Session 3: Environmental and Medical Genomics 15.20-15.40 Break 15.40-17.00 Session 3, continued 17.00-19.00 Poster Session I and Drinks Reception 19.00-21.00 Dinner Friday 17th September 2010 07.30-09.00 Breakfast 09.00-10.20 Session 4: Databases, Data Mining, Visualization and Curation 10.20-10.40 Morning Coffee 10.40-12.00 Session 4, continued 12.00-14.00 Lunch 14.00-16.00 Free afternoon 16.00-17.00 Keynote Speaker: Alex Bateman 17.00-19.00 Poster Session II and Drinks Reception 19.00-21.00 Dinner Saturday 18th September 2010 07.30-09.00 Breakfast 09.00-10.20 Session 5: Sequencing Pipelines and Assembly 10.20-10.40
[Show full text]
Coregulation of Pathways in Lung Cancer Patients With
British Journal of Cancer www.nature.com/bjc REVIEW ARTICLE Translational Therapeutics Coregulation of pathways in lung cancer patients with EGFR mutation: therapeutic opportunities ✉ Rafael Rosell 1,2 , Andrés Felipe Cardona3, Oscar Arrieta4,5, Andrés Aguilar2, Masaoki Ito6, Carlos Pedraz7,8, Jordi Codony-Servat9 and Mariacarmela Santarpia10 © The Author(s), under exclusive licence to Springer Nature Limited 2021 Epidermal growth factor receptor (EGFR) mutations in lung adenocarcinoma are a frequent class of driver mutations. Single EGFR tyrosine kinase inhibitor (TKI) provides substantial clinical beneﬁt, but almost nil radiographic complete responses. Patients invariably progress, although survival can reach several years with post-treatment therapies, including EGFR TKIs, chemotherapy or other procedures. Endeavours have been clinically oriented to manage the acquisition of EGFR TKI-resistant mutations; however, basic principles on cancer evolution have not been considered in clinical trials. For years, evidence has displayed rapidly adaptive mechanisms of resistance to selective monotherapy, posing several dilemmas for the practitioner. Strict adherence to non-small cell lung cancer (NSCLC) guidelines is not always practical for addressing the clinical progression that EGFR-mutant lung adenocarcinoma patients suffer. The purpose of this review is to highlight regulatory mechanisms and signalling pathways that cause therapy-induced resistance to EGFR TKIs. It suggests combinatorial therapies that target EGFR, as well as potential mechanisms underlying EGFR-mutant NSCLC, alerting the reader to clinical opportunities that may lead to a deeper and more durable response. Molecular reprogramming contributes to EGFR TKI resistance, and the compiled information is relevant in understanding the development of new combined targeted strategies in EGFR-mutant NSCLC.
[Show full text]
Perfect Conserved Linkage Across the Entire Mouse Chromosome 10 Region Homologous to Human Chromosome 21
Downloaded from genome.cshlp.org on October 1, 2021 - Published by Cold Spring Harbor Laboratory Press Letter Perfect Conserved Linkage Across the Entire Mouse Chromosome 10 Region Homologous to Human Chromosome 21 Tim Wiltshire,1,2,5 Mathew Pletcher,1,5 Susan E. Cole,1,3 Melissa Villanueva,1 Bruce Birren,4 Jessica Lehoczky,4 Ken Dewar,4 and Roger H. Reeves1,6 1Department of Physiology, Johns Hopkins School of Medicine, Baltimore, Maryland 21205 USA; 4Whitehead Institute/MIT Center for Genome Research, Cambridge, Massachusetts 02141 USA The distal end of human Chromosome (HSA) 21 from PDXK to the telomere shows perfect conserved linkage with mouse Chromosome (MMU) 10. This region is bounded on the proximal side by a segment of homology to HSA22q11.2, and on the distal side by a region of homology with HSA19p13.1. A high-resolution PAC-based physical map is described that spans 2.8 Mb, including the entire 2.1 Mb from Pdxk to Prmt2 corresponding to HSA21. Thirty-four expressed sequences are mapped, three of which were not mapped previously in any species and nine more that are mapped in mouse for the first time. These genes confirm and extend the conserved linkage between MMU10 and HSA21. The ordered PACs and dense STS map provide a clone resource for biological experiments, for rapid and accurate mapping, and for genomic sequencing. The new genes identified here may be involved in Down syndrome (DS) or in several genetic diseases that map to this conserved region of HSA21. Trisomy 21 is the most frequent human aneuploidy at HSA21, several lines of evidence suggest that this chro- birth, occurring in 1 out of 700 live births (Hassold et mosome may have a lower gene density than other al.
[Show full text]
Package 'Dasir'
Package ‘DASiR’ October 7, 2014 Type Package Title Distributed Annotation System in R Version 1.4.0 Date 2013-06-14 Author Oscar Flores, Anna Mantsoki Maintainer Oscar Flores <[email protected]>, Anna Mantsoki <[email protected]> Description R package for programmatic retrieval of information from DAS servers License LGPL (>= 3) Depends IRanges, GenomicRanges, XML, Biostrings LazyLoad yes biocViews Annotation R topics documented: DASiR-package . .2 getDas-functions . .4 getDasFeature . .6 getDasSequence . .7 getDasStructure . .8 plotFeatures . 10 Index 12 1 2 DASiR-package DASiR-package Distributed Annotation System in R Description R package for programmatic retrieval of information from DAS servers Details Package: DASiR Type: Package License: LGPL(>= 3) Distributed Annotation System (DAS) is a protocol for information exchange between a server and a client. Is widely used in bioinformatics and the most important repositories include a DAS server parallel to their main front-end. DAS uses XML and HTTP protocols, so the requirements are much less than using MySQL or BioMart based alternatives. This package provides a convenient R-DAS interface to programmatically access DAS servers avail- able from your network. It supports only the basic features of DAS 1.6 protocol (DAS/2 is not supported) but these should be enough for most of the users. Despite a large number (>1200 according ofﬁcial numbers on February 2013) are available, this package is designed with range-features (neither coverages nor sequences). DAS also supports querying genomic sequences and protein structures, but there are already better ways to access such static data in R. In order to start with this package, you can give a look to basic metadata functions in getDas-functions man page and to the main functions getDasFeature,getDasSequence, getDasStructure.
[Show full text]
Computational Protein Design: Assessment And
COMPUTATIONAL PROTEIN DESIGN: ASSESSMENT AND APPLICATIONS Zhixiu Li Submitted to the faculty of University Graduate School in partial fulfillment of the requirements for the degree Doctor of Philosophy in the School of Informatics and Computing, Indiana University May 2015 Accepted by the Graduate Faculty, Indiana University, in partial fulfillment of the requirements for the degree of Doctor of Philosophy. ________________________________ Yunlong Liu, PhD, Chair ________________________________ Huanmei Wu, PhD Doctoral Committee ________________________________ Samy Meroueh, PhD November 24, 2014 ________________________________ Yaoqi Zhou, PhD ii © 2015 Zhixiu Li iii DEDICATION Dedicated to my family and friends. iv ACKNOWLEDGEMENTS I would like to thank my research committee members, my family and friends for their help in my Ph.D study. Foremost, I would like to express my sincere gratitude to my advisor Prof Yaoqi Zhou. He has provided me excellent research advice, great insights, enthusiasm and encouragement throughout all my research projects. His guidance and support help all the time in research and dissertation writing. I would never have been able to finish my dissertation without his help. Besides my advisor, I would like to extend my sincerest thanks and appreciation the rest of my research committee: Profs Yunlong Liu, Samy Meroueh, and Huanmei Wu, for all the useful discussions, encouragement, and insightful comments. I also want to thank my colleagues, collaborators, teachers and classmates in various projects. I shared a great time with them while learning from them. They are Profs Qizhuang Ye, Song Liu, Shiaofen Fang, Mohammad Al Hasan, James H. Hill, Jihua Wang, Drs Yuedong Yang, Huiying Zhao, Jian Zhan, Tuo Zhang, Liang Dai, Eshel Faraggi, Wenchang Xiang, Hui Huang, Md Tamjdul Hogue, Mr.
[Show full text]
High-Depth African Genomes Inform Human Migration and Health
Article High-depth African genomes inform human migration and health https://doi.org/10.1038/s41586-020-2859-7 Ananyo Choudhury1, Shaun Aron1, Laura R. Botigué2, Dhriti Sengupta1, Gerrit Botha3, Taoufik Bensellak4, Gordon Wells5,6, Judit Kumuthini5,6, Daniel Shriner7, Yasmina J. Fakim8,9, Received: 10 May 2019 Anisah W. Ghoorah9, Eileen Dareng10,11, Trust Odia12, Oluwadamilare Falola12, Ezekiel Adebiyi12,13, Accepted: 7 August 2020 Scott Hazelhurst1,14, Gaston Mazandu3, Oscar A. Nyangiri15, Mamana Mbiyavanga3, Alia Benkahla16, Samar K. Kassim17, Nicola Mulder3, Sally N. Adebamowo18,19, Published online: 28 October 2020 Emile R. Chimusa20, Donna Muzny21, Ginger Metcalf21, Richard A. Gibbs21,22, Open access TrypanoGEN Research Group*, Charles Rotimi7, Michèle Ramsay1,23, H3Africa Consortium*, Adebowale A. Adeyemo7 ✉, Zané Lombard23 ✉ & Neil A. Hanchard22 ✉ Check for updates The African continent is regarded as the cradle of modern humans and African genomes contain more genetic variation than those from any other continent, yet only a fraction of the genetic diversity among African individuals has been surveyed1. Here we performed whole-genome sequencing analyses of 426 individuals— comprising 50 ethnolinguistic groups, including previously unsampled populations—to explore the breadth of genomic diversity across Africa. We uncovered more than 3 million previously undescribed variants, most of which were found among individuals from newly sampled ethnolinguistic groups, as well as 62 previously unreported loci that are under strong selection, which were predominantly found in genes that are involved in viral immunity, DNA repair and metabolism. We observed complex patterns of ancestral admixture and putative-damaging and novel variation, both within and between populations, alongside evidence that Zambia was a likely intermediate site along the routes of expansion of Bantu-speaking populations.
[Show full text]
3 Meta-Analysis of Genome- Wide Association Studies for Neuroticism in 449,484 Individuals Identifies Novel Genetic Loci and Pathways
Changing perspectives Towards detailed phenotyping in genetics Mats Nagel Ó Mats Nagel, 2020 All rights reserved. The research in this thesis was supported by a grant from the Netherlands Organization for Scientific Research, project number 452-12-014. Cover design: Mats Nagel Cover photo: Vern Dewit Printing: Off Page ISBN: 978-94-93197-07-7 DOI: 10.31237/osf.io/a4nz2 VRIJE UNIVERSITEIT Changing perspectives Towards detailed phenotyping in genetics ACADEMISCH PROEFSCHRIFT ter verkrijging van de graad Doctor of Philosophy aan de Vrije Universiteit Amsterdam, op gezag van de rector magnificus prof.dr. V. Subramaniam, in het openbaar te verdedigen ten overstaan van de promotiecommissie van de Faculteit der Bètawetenschappen op dinsdag 30 juni 2020 om 13.45 uur in een online bijeenkomst van de universiteit, De Boelelaan 1105 door Mats Nagel geboren te Amsterdam promotor: prof.dr. D.P. Posthuma copromotor: dr. S. van der Sluis Leescommissie: prof.dr. H. D. Mansvelder prof. C. M. Lewis prof.dr. B. W. J. H. Penninx dr. E. I. Fried dr. M. G. Nivard Paranimfen: Oscar van Mourik Philip R. Jansen Contents 1 General introduction 9 1.1 Brief introduction 10 1.2 Background 11 1.3 Genetic research into psychological traits 15 1.4 Aims and outline of this thesis 24 1.5 Glossary 27 2 Item-level analyses reveal genetic heterogeneity in neuroticism 31 Abstract 32 2.1 Introduction 33 2.2 Results 34 2.3 Discussion 43 2.4 Methods 44 2.5 Supplementary information 50 3 Meta-analysis of genome-wide association studies for neuroticism in 449,484 individuals identifies
[Show full text]