DOCSLIB.ORG

MS4A2 and FCER1A , and GATA2

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
MS4A2 and FCER1A , and GATA2 Critical Roles for PU.1, GATA1, and GATA2 in the Expression of Human Fc εRI on Mast Cells: PU.1 and GATA1 Transactivate FCER1A, and GATA2 Transactivates This information is current as FCER1A and MS4A2 of September 28, 2021. Eisuke Inage, Kazumi Kasakura, Takuya Yashiro, Ryuyo Suzuki, Yosuke Baba, Nobuhiro Nakano, Mutsuko Hara, Atsushi Tanabe, Keisuke Oboki, Kenji Matsumoto, Hirohisa Saito, François Niyonsaba, Yoshikazu Ohtsuka, Hideoki Downloaded from Ogawa, Ko Okumura, Toshiaki Shimizu and Chiharu Nishiyama J Immunol published online 17 March 2014 http://www.jimmunol.org/content/early/2014/03/17/jimmun ol.1302366 http://www.jimmunol.org/ Supplementary http://www.jimmunol.org/content/suppl/2014/03/17/jimmunol.130236 Material 6.DCSupplemental Why The JI? Submit online. by guest on September 28, 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 © 2014 by The American Association of Immunologists, Inc. All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. Published March 17, 2014, doi:10.4049/jimmunol.1302366 The Journal of Immunology Critical Roles for PU.1, GATA1, and GATA2 in the Expression of Human Fc«RI on Mast Cells: PU.1 and GATA1 Transactivate FCER1A, and GATA2 Transactivates FCER1A and MS4A2 Eisuke Inage,*,†,1 Kazumi Kasakura,*,‡,1 Takuya Yashiro,*,‡ Ryuyo Suzuki,† Yosuke Baba,*,† Nobuhiro Nakano,* Mutsuko Hara,* Atsushi Tanabe,* Keisuke Oboki,x,{ Kenji Matsumoto,x Hirohisa Saito,x Franc¸ois Niyonsaba,* Yoshikazu Ohtsuka,† Hideoki Ogawa,* Ko Okumura,* Toshiaki Shimizu,† and Chiharu Nishiyama*,‡ The high-affinity IgE receptor, Fc«RI, which is composed of a-, b-, and g-chains, plays an important role in IgE-mediated allergic Downloaded from responses. In the current study, involvement of the transcription factors, PU.1, GATA1, and GATA2, in the expression of Fc«RI on human mast cells was investigated. Transfection of small interfering RNAs (siRNAs) against PU.1, GATA1, and GATA2 into the human mast cell line, LAD2, caused significant downregulation of cell surface expression of Fc«RI. Quantification of the mRNA levels revealed that PU.1, GATA1, and GATA2 siRNAs suppressed the a transcript, whereas the amount of b mRNA was reduced in only GATA2 siRNA transfectants. In contrast, g mRNA levels were not affected by any of the knockdowns. Chromatin immunoprecipitation assay showed that significant amounts of PU.1, GATA1, and GATA2 bind to the promoter region of FCER1A http://www.jimmunol.org/ (encoding Fc«RIa) and that GATA2 binds to the promoter of MS4A2 (encoding Fc«RIb). Luciferase assay and EMSA showed that GATA2 transactivates the MS4A2 promoter via direct binding. These knockdowns of transcription factors also suppressed the IgE-mediated degranulation activity of LAD2. Similarly, all three knockdowns suppressed Fc«RI expression in primary mast cells, especially PU.1 siRNA and GATA2 siRNA, which target Fc«RIa and Fc«RIb, respectively. From these results, we conclude that PU.1 and GATA1 are involved in Fc«RIa transcription through recruitment to its promoter, whereas GATA2 positively regulates Fc«RIb transcription. Suppression of these transcription factors leads to downregulation of Fc«RI expression and IgE- mediated degranulation activity. Our findings will contribute to the development of new therapeutic approaches for Fc«RI- mediated allergic diseases. The Journal of Immunology, 2014, 192: 000–000. by guest on September 28, 2021 he high-affinity IgE receptor, FcεRI, plays a crucial role cells, including rapid degranulation, immediate eicosanoid gen- in various IgE-mediated responses, including allergic dis- eration, and transcription of cytokine genes. FcεRI expression T eases and host defense against parasites. Mast cells and levels on the cell surface affect the magnitude of IgE-mediated basophils are the major effector cells expressing FcεRI, whose responses. In the case of allergic patients carrying high serum IgE cross-linking by IgE and multivalent Ags causes stimulation of value, FcεRI on the cell surface is occupied by an IgE Ab a priori. In addition to its role as a trigger of allergen-induced stimulation of cells, the interaction between IgE and FcεRI is involved in the *Atopy (Allergy) Research Center, Juntendo University School of Medicine, Tokyo, enhancement of allergic responses, even in the absence of cross- 113-8421, Japan; †Department of Pediatrics and Adolescent Medicine, Juntendo ‡ linking by allergens, by at least two mechanisms, as follows: 1) University School of Medicine, Tokyo, 113-8421, Japan; Department of Biological ε Science and Technology, Faculty of Industrial Science and Technology, Tokyo Uni- the binding of monomeric IgE to Fc RI increases the amount of versity of Science, Tokyo, 125-8585, Japan; xNational Research Institute for Child ε { cell surface Fc RI (1); and 2) the binding of monomeric IgE Health and Development, Tokyo, 157-8535, Japan; and Department of Molecular to FcεRI enhances cell viability (2, 3). Uncovering the mechanism Medical Research, Tokyo Metropolitan Institute of Medical Science, Tokyo, 156- 8506, Japan of FcεRI expression will be important for finding ways to control 1 ε E.I. and K.K. contributed equally to this work. Fc RI expression, with a view to suppressing allergic responses. ε Received for publication September 5, 2013. Accepted for publication February 11, Fc RI is composed of three subunits, as follows: a, the IgE- 2014. binding subunit; and b and g, the signal transduction subunits. In This work was supported by the Funding Program for Next Generation World- our previous studies regarding the transcriptional regulation of Leading Researchers from the Ministry of Education, Culture, Sports, Science, and FcεRI subunit genes, several transcription factors have been Technology of Japan (to C.N.). T.Y. is a Japan Society for the Promotion of Science Research Fellow. identified (4–9). Among them, hematopoietic cell-specific tran- scription factors are known to be involved in mast cell/basophil- Address correspondence and reprint requests to Prof. Chiharu Nishiyama, Depart- ment of Biological Science and Technology, Faculty of Industrial Science and Tech- specific gene regulation. Briefly, cooperation between PU.1 and nology, Tokyo University of Science, 6-3-1 Niijuku, Katsushika-ku, Tokyo, 125- GATA1 in FcεRI-positive cells (5), and the suppressive effect of 8585, Japan. E-mail address: [email protected] FOG-1 on GATA1 in FcεRI-negative cells (7), determines the cell The online version of this article contains supplemental material. type–specific expression of human a and mouse b genes, re- Abbreviations used in this article: BMMC, bone marrow–derived mast cell; ChIP, spectively. In these previous studies, reporter assays and EMSAs chromatin immunoprecipitation; NP, nitrophenyl; siRNA, small interfering RNA. were mainly used to identify and to analyze the role of the tran- Copyright Ó 2014 by The American Association of Immunologists, Inc. 0022-1767/14/$16.00 scription factors regulating the promoter activation. In contrast, www.jimmunol.org/cgi/doi/10.4049/jimmunol.1302366 2 INVOLVEMENT OF PU.1, GATA1, AND GATA2 IN HUMAN FcεRI EXPRESSION the involvement of GATA1 and GATA2 in the expression of FcεRI sciences) and rabbit IgG (02-6102; Invitrogen) were used as control Abs. was denied in some studies using mouse bone marrow–derived The amount of chromosomal DNA, including promoters of FcεRIa, b, mast cells (BMMCs) and/or the rat basophilic leukemia cell line, and g, was determined by the TaqMan system using the primers and TaqMan probes listed in Supplemental Table E1. RBL-2H3 (10, 11). Therefore, in the current study, we analyzed the involvement of PU.1, GATA1, and GATA2 in FcεRI expres- Luciferase assay sion in the human mast cell line LAD2 and primary human mast MS4A2 promoter regions were amplified from human genomic DNA by cells using small interfering RNA (siRNA) and the chromatin using PCR and inserted into the multicloning site of pGL-4 Basic (Promega, immunoprecipitation (ChIP) assay to verify our previous findings. Madison, WI) to generate reporter plasmids. The nucleotide sequences of This report demonstrates that PU.1, GATA1, and GATA2 are primer sets are listed in Supplemental Table E2. The expression plasmids ε pCR-GATA1 (4) and pCR-GATA2 (18), which were generated in our pre- positive regulators of the expression and function of Fc RI in vious studies, and their empty vector pCR3.1 (Invitrogen), were used in human mast cells. We newly identified GATA2 as a critical trans- this study. HEK293T cells (human embryonic kidney cell line) were trans- activator of the human Fc«RIb promoter, whose cell type–specific fected with 500 ng reporter plasmid, 500 ng expression plasmid, and 10 ng transcription factors have not been reported to date. Additionally, pRL-null (Promega) with FuGENE HD (Roche Diagnostics, Indianapolis, we showed that FcεRIa expression was induced by GATA2 as IN). Luciferase activity
Load more

Recommended publications
  • Viewed Under 23 (B) Or 203 (C) fi M M Male Cko Mice, and Largely Unaffected Magni Cation; Scale Bars, 500 M (B) and 50 M (C)
    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.
    [Show full text]
  • Table 2. Significant
    Table 2. Significant (Q < 0.05 and |d | > 0.5) transcripts from the meta-analysis Gene Chr Mb Gene Name Affy ProbeSet cDNA_IDs d HAP/LAP d HAP/LAP d d IS Average d Ztest P values Q-value Symbol ID (study #5) 1 2 STS B2m 2 122 beta-2 microglobulin 1452428_a_at AI848245 1.75334941 4 3.2 4 3.2316485 1.07398E-09 5.69E-08 Man2b1 8 84.4 mannosidase 2, alpha B1 1416340_a_at H4049B01 3.75722111 3.87309653 2.1 1.6 2.84852656 5.32443E-07 1.58E-05 1110032A03Rik 9 50.9 RIKEN cDNA 1110032A03 gene 1417211_a_at H4035E05 4 1.66015788 4 1.7 2.82772795 2.94266E-05 0.000527 NA 9 48.5 --- 1456111_at 3.43701477 1.85785922 4 2 2.8237185 9.97969E-08 3.48E-06 Scn4b 9 45.3 Sodium channel, type IV, beta 1434008_at AI844796 3.79536664 1.63774235 3.3 2.3 2.75319499 1.48057E-08 6.21E-07 polypeptide Gadd45gip1 8 84.1 RIKEN cDNA 2310040G17 gene 1417619_at 4 3.38875643 1.4 2 2.69163229 8.84279E-06 0.0001904 BC056474 15 12.1 Mus musculus cDNA clone 1424117_at H3030A06 3.95752801 2.42838452 1.9 2.2 2.62132809 1.3344E-08 5.66E-07 MGC:67360 IMAGE:6823629, complete cds NA 4 153 guanine nucleotide binding protein, 1454696_at -3.46081884 -4 -1.3 -1.6 -2.6026947 8.58458E-05 0.0012617 beta 1 Gnb1 4 153 guanine nucleotide binding protein, 1417432_a_at H3094D02 -3.13334396 -4 -1.6 -1.7 -2.5946297 1.04542E-05 0.0002202 beta 1 Gadd45gip1 8 84.1 RAD23a homolog (S.
    [Show full text]
  • Elements of Immunoglobulin E Network Associate with Aortic Valve Area in Patients with Acquired Aortic Stenosis
    biomedicines Communication Elements of Immunoglobulin E Network Associate with Aortic Valve Area in Patients with Acquired Aortic Stenosis Daniel P. Potaczek 1,2,† , Aleksandra Przytulska-Szczerbik 2,†, Stanisława Bazan-Socha 3 , Artur Jurczyszyn 4, Ko Okumura 5, Chiharu Nishiyama 6, Anetta Undas 2,7,‡ and Ewa Wypasek 2,8,*,‡ 1 Translational Inflammation Research Division & Core Facility for Single Cell Multiomics, Medical Faculty, Philipps University Marburg, Member of the German Center for Lung Research (DZL) and the Universities of Giessen and Marburg Lung Center, 35043 Marburg, Germany; [email protected] 2 Krakow Center for Medical Research and Technology, John Paul II Hospital, 31-202 Krakow, Poland; [email protected] (A.P.-S.); [email protected] (A.U.) 3 Department of Internal Medicine, Jagiellonian University Medical College, 31-066 Krakow, Poland; [email protected] 4 Department of Hematology, Jagiellonian University Medical College, 31-501 Krakow, Poland; [email protected] 5 Atopy Research Center, Juntendo University School of Medicine, Tokyo 113-8421, Japan; [email protected] 6 Laboratory of Molecular Biology and Immunology, Department of Biological Science and Technology, Tokyo University of Science, Tokyo 125-8585, Japan; [email protected] 7 Institute of Cardiology, Jagiellonian University Medical College, 31-202 Krakow, Poland 8 Faculty of Medicine and Health Sciences, Andrzej Frycz Modrzewski Krakow University, 30-705 Krakow, Poland * Correspondence: [email protected]; Tel.: +48-12-614-31-35 † These first authors contributed equally to this work. ‡ These last authors contributed equally to this work. Abstract: Allergic mechanisms are likely involved in atherosclerosis and its clinical presentations, Citation: Potaczek, D.P.; Przytulska-Szczerbik, A.; Bazan-Socha, such as coronary artery disease (CAD).
    [Show full text]
  • Supplementary Material DNA Methylation in Inflammatory Pathways Modifies the Association Between BMI and Adult-Onset Non- Atopic
    Supplementary Material DNA Methylation in Inflammatory Pathways Modifies the Association between BMI and Adult-Onset Non- Atopic Asthma Ayoung Jeong 1,2, Medea Imboden 1,2, Akram Ghantous 3, Alexei Novoloaca 3, Anne-Elie Carsin 4,5,6, Manolis Kogevinas 4,5,6, Christian Schindler 1,2, Gianfranco Lovison 7, Zdenko Herceg 3, Cyrille Cuenin 3, Roel Vermeulen 8, Deborah Jarvis 9, André F. S. Amaral 9, Florian Kronenberg 10, Paolo Vineis 11,12 and Nicole Probst-Hensch 1,2,* 1 Swiss Tropical and Public Health Institute, 4051 Basel, Switzerland; [email protected] (A.J.); [email protected] (M.I.); [email protected] (C.S.) 2 Department of Public Health, University of Basel, 4001 Basel, Switzerland 3 International Agency for Research on Cancer, 69372 Lyon, France; [email protected] (A.G.); [email protected] (A.N.); [email protected] (Z.H.); [email protected] (C.C.) 4 ISGlobal, Barcelona Institute for Global Health, 08003 Barcelona, Spain; [email protected] (A.-E.C.); [email protected] (M.K.) 5 Universitat Pompeu Fabra (UPF), 08002 Barcelona, Spain 6 CIBER Epidemiología y Salud Pública (CIBERESP), 08005 Barcelona, Spain 7 Department of Economics, Business and Statistics, University of Palermo, 90128 Palermo, Italy; [email protected] 8 Environmental Epidemiology Division, Utrecht University, Institute for Risk Assessment Sciences, 3584CM Utrecht, Netherlands; [email protected] 9 Population Health and Occupational Disease, National Heart and Lung Institute, Imperial College, SW3 6LR London, UK; [email protected] (D.J.); [email protected] (A.F.S.A.) 10 Division of Genetic Epidemiology, Medical University of Innsbruck, 6020 Innsbruck, Austria; [email protected] 11 MRC-PHE Centre for Environment and Health, School of Public Health, Imperial College London, W2 1PG London, UK; [email protected] 12 Italian Institute for Genomic Medicine (IIGM), 10126 Turin, Italy * Correspondence: [email protected]; Tel.: +41-61-284-8378 Int.
    [Show full text]
  • Microarray Analysis of Novel Genes Involved in HSV- 2 Infection
    Microarray analysis of novel genes involved in HSV- 2 infection Hao Zhang Nanjing University of Chinese Medicine Tao Liu ( [email protected] ) Nanjing University of Chinese Medicine https://orcid.org/0000-0002-7654-2995 Research Article Keywords: HSV-2 infection,Microarray analysis,Histospecic gene expression Posted Date: May 12th, 2021 DOI: https://doi.org/10.21203/rs.3.rs-517057/v1 License: This work is licensed under a Creative Commons Attribution 4.0 International License. Read Full License Page 1/19 Abstract Background: Herpes simplex virus type 2 infects the body and becomes an incurable and recurring disease. The pathogenesis of HSV-2 infection is not completely clear. Methods: We analyze the GSE18527 dataset in the GEO database in this paper to obtain distinctively displayed genes(DDGs)in the total sequential RNA of the biopsies of normal and lesioned skin groups, healed skin and lesioned skin groups of genital herpes patients, respectively.The related data of 3 cases of normal skin group, 4 cases of lesioned group and 6 cases of healed group were analyzed.The histospecic gene analysis , functional enrichment and protein interaction network analysis of the differential genes were also performed, and the critical components were selected. Results: 40 up-regulated genes and 43 down-regulated genes were isolated by differential performance assay. Histospecic gene analysis of DDGs suggested that the most abundant system for gene expression was the skin, immune system and the nervous system.Through the construction of core gene combinations, protein interaction network analysis and selection of histospecic distribution genes, 17 associated genes were selected CXCL10,MX1,ISG15,IFIT1,IFIT3,IFIT2,OASL,ISG20,RSAD2,GBP1,IFI44L,DDX58,USP18,CXCL11,GBP5,GBP4 and CXCL9.The above genes are mainly located in the skin, immune system, nervous system and reproductive system.
    [Show full text]
  • GATA2 Regulates Mast Cell Identity and Responsiveness to Antigenic Stimulation by Promoting Chromatin Remodeling at Super- Enhancers
    ARTICLE https://doi.org/10.1038/s41467-020-20766-0 OPEN GATA2 regulates mast cell identity and responsiveness to antigenic stimulation by promoting chromatin remodeling at super- enhancers Yapeng Li1, Junfeng Gao 1, Mohammad Kamran1, Laura Harmacek2, Thomas Danhorn 2, Sonia M. Leach1,2, ✉ Brian P. O’Connor2, James R. Hagman 1,3 & Hua Huang 1,3 1234567890():,; Mast cells are critical effectors of allergic inflammation and protection against parasitic infections. We previously demonstrated that transcription factors GATA2 and MITF are the mast cell lineage-determining factors. However, it is unclear whether these lineage- determining factors regulate chromatin accessibility at mast cell enhancer regions. In this study, we demonstrate that GATA2 promotes chromatin accessibility at the super-enhancers of mast cell identity genes and primes both typical and super-enhancers at genes that respond to antigenic stimulation. We find that the number and densities of GATA2- but not MITF-bound sites at the super-enhancers are several folds higher than that at the typical enhancers. Our studies reveal that GATA2 promotes robust gene transcription to maintain mast cell identity and respond to antigenic stimulation by binding to super-enhancer regions with dense GATA2 binding sites available at key mast cell genes. 1 Department of Immunology and Genomic Medicine, National Jewish Health, Denver, CO 80206, USA. 2 Center for Genes, Environment and Health, National Jewish Health, Denver, CO 80206, USA. 3 Department of Immunology and Microbiology, University of Colorado Anschutz Medical Campus, Aurora, ✉ CO 80045, USA. email: [email protected] NATURE COMMUNICATIONS | (2021) 12:494 | https://doi.org/10.1038/s41467-020-20766-0 | www.nature.com/naturecommunications 1 ARTICLE NATURE COMMUNICATIONS | https://doi.org/10.1038/s41467-020-20766-0 ast cells (MCs) are critical effectors in immunity that at key MC genes.
    [Show full text]
  • Supplementary Table 2
    Supplementary Table 2. Differentially Expressed Genes following Sham treatment relative to Untreated Controls Fold Change Accession Name Symbol 3 h 12 h NM_013121 CD28 antigen Cd28 12.82 BG665360 FMS-like tyrosine kinase 1 Flt1 9.63 NM_012701 Adrenergic receptor, beta 1 Adrb1 8.24 0.46 U20796 Nuclear receptor subfamily 1, group D, member 2 Nr1d2 7.22 NM_017116 Calpain 2 Capn2 6.41 BE097282 Guanine nucleotide binding protein, alpha 12 Gna12 6.21 NM_053328 Basic helix-loop-helix domain containing, class B2 Bhlhb2 5.79 NM_053831 Guanylate cyclase 2f Gucy2f 5.71 AW251703 Tumor necrosis factor receptor superfamily, member 12a Tnfrsf12a 5.57 NM_021691 Twist homolog 2 (Drosophila) Twist2 5.42 NM_133550 Fc receptor, IgE, low affinity II, alpha polypeptide Fcer2a 4.93 NM_031120 Signal sequence receptor, gamma Ssr3 4.84 NM_053544 Secreted frizzled-related protein 4 Sfrp4 4.73 NM_053910 Pleckstrin homology, Sec7 and coiled/coil domains 1 Pscd1 4.69 BE113233 Suppressor of cytokine signaling 2 Socs2 4.68 NM_053949 Potassium voltage-gated channel, subfamily H (eag- Kcnh2 4.60 related), member 2 NM_017305 Glutamate cysteine ligase, modifier subunit Gclm 4.59 NM_017309 Protein phospatase 3, regulatory subunit B, alpha Ppp3r1 4.54 isoform,type 1 NM_012765 5-hydroxytryptamine (serotonin) receptor 2C Htr2c 4.46 NM_017218 V-erb-b2 erythroblastic leukemia viral oncogene homolog Erbb3 4.42 3 (avian) AW918369 Zinc finger protein 191 Zfp191 4.38 NM_031034 Guanine nucleotide binding protein, alpha 12 Gna12 4.38 NM_017020 Interleukin 6 receptor Il6r 4.37 AJ002942
    [Show full text]
  • MS4A1 Monoclonal Antibody, Clone LT20
    MS4A1 monoclonal antibody, clone Storage Instruction: Store in the dark at 4°C. Do not LT20 (APC) freeze. Avoid prolonged exposure to light. Catalog Number: MAB4383 Aliquot to avoid repeated freezing and thawing. Regulatory Status: For research use only (RUO) Entrez GeneID: 931 Product Description: Mouse monoclonal antibody Gene Symbol: MS4A1 raised against native MS4A1. Gene Alias: B1, Bp35, CD20, LEU-16, MGC3969, Clone Name: LT20 MS4A2, S7 Immunogen: Native purified MS4A1 from normal human Gene Summary: This gene encodes a member of the lymphocytes from lymph node. membrane-spanning 4A gene family. Members of this nascent protein family are characterized by common Host: Mouse structural features and similar intron/exon splice boundaries and display unique expression patterns Theoretical MW (kDa): 33-37 among hematopoietic cells and nonlymphoid tissues. This gene encodes a B-lymphocyte surface molecule Reactivity: Human which plays a role in the development and differentiation of B-cells into plasma cells. This family member is Applications: Flow Cyt localized to 11q12, among a cluster of family members. (See our web site product page for detailed applications Alternative splicing of this gene results in two transcript information) variants which encode the same protein. [provided by RefSeq] Protocols: See our web site at http://www.abnova.com/support/protocols.asp or product References: page for detailed protocols 1. The biological activity of human CD20 monoclonal antibodies is linked to unique epitopes on CD20. Teeling Specificity: This antibody reacts with CD20 (Bp35), a JL, Mackus WJ, Wiegman LJ, van den Brakel JH, Beers 33-37 KDa non-glycosylated membrane receptor with SA, French RR, van Meerten T, Ebeling S, Vink T, four transmembrane domains, expressed on B Slootstra JW, Parren PW, Glennie MJ, van de Winkel lymphocytes (it is lost on plasma cells), follicular JG.
    [Show full text]
  • FCER1A Monoclonal Antibody, Clone CRA1
    FCER1A monoclonal antibody, hay fever and asthma. The allergic response occurs clone CRA1 when 2 or more high-affinity IgE receptors are crosslinked via IgE molecules that in turn are bound to Catalog Number: MAB7943 an allergen (antigen) molecule. A perturbation occurs that brings about the release of histamine and proteases Regulatory Status: For research use only (RUO) from the granules in the cytoplasm of the mast cell and leads to the synthesis of prostaglandins and Product Description: Mouse monoclonal antibody leukotrienes--potent effectors of the hypersensitivity raised against recombinant FCER1A. response. The IgE receptor consists of 3 subunits: alpha, beta (MIM 147138), and gamma (MIM 147139); Clone Name: CRA1 only the alpha subunit is glycosylated.[supplied by OMIM] Immunogen: Recombinant protein corresponding to human FCER1A. References: 1. IgE- and FcepsilonRI-mediated migration of human Host: Mouse basophils. Suzukawa M, Hirai K, Iikura M, Nagase H, Komiya A, Yoshimura-Uchiyama C, Yamada H, Ra C, Reactivity: Human Ohta K, Yamamoto K, Yamaguchi M. Int Immunol. 2005 Applications: Flow Cyt, IHC, WB Sep;17(9):1249-55. Epub 2005 Aug 15. (See our web site product page for detailed applications 2. IgE enhances Fc epsilon receptor I expression and information) IgE-dependent release of histamine and lipid mediators from human umbilical cord blood-derived mast cells: Protocols: See our web site at synergistic effect of IL-4 and IgE on human mast cell Fc http://www.abnova.com/support/protocols.asp or product epsilon receptor I expression and mediator release. page for detailed protocols Yamaguchi M, Sayama K, Yano K, Lantz CS, Noben-Trauth N, Ra C, Costa JJ, Galli SJ.
    [Show full text]
  • Comprehensive Analysis Reveals Novel Gene Signature in Head and Neck Squamous Cell Carcinoma: Predicting Is Associated with Poor Prognosis in Patients
    5892 Original Article Comprehensive analysis reveals novel gene signature in head and neck squamous cell carcinoma: predicting is associated with poor prognosis in patients Yixin Sun1,2#, Quan Zhang1,2#, Lanlin Yao2#, Shuai Wang3, Zhiming Zhang1,2 1Department of Breast Surgery, The First Affiliated Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, China; 2School of Medicine, Xiamen University, Xiamen, China; 3State Key Laboratory of Cellular Stress Biology, School of Life Sciences, Xiamen University, Xiamen, China Contributions: (I) Conception and design: Y Sun, Q Zhang; (II) Administrative support: Z Zhang; (III) Provision of study materials or patients: Y Sun, Q Zhang; (IV) Collection and assembly of data: Y Sun, L Yao; (V) Data analysis and interpretation: Y Sun, S Wang; (VI) Manuscript writing: All authors; (VII) Final approval of manuscript: All authors. #These authors contributed equally to this work. Correspondence to: Zhiming Zhang. Department of Surgery, The First Affiliated Hospital of Xiamen University, Xiamen, China. Email: [email protected]. Background: Head and neck squamous cell carcinoma (HNSC) remains an important public health problem, with classic risk factors being smoking and excessive alcohol consumption and usually has a poor prognosis. Therefore, it is important to explore the underlying mechanisms of tumorigenesis and screen the genes and pathways identified from such studies and their role in pathogenesis. The purpose of this study was to identify genes or signal pathways associated with the development of HNSC. Methods: In this study, we downloaded gene expression profiles of GSE53819 from the Gene Expression Omnibus (GEO) database, including 18 HNSC tissues and 18 normal tissues.
    [Show full text]
  • Role of Epistasis in Alzheimer's Disease Genetics
    Brigham Young University BYU ScholarsArchive Theses and Dissertations 2014-12-01 Role of Epistasis in Alzheimer's Disease Genetics Mark T. Ebbert Brigham Young University - Provo Follow this and additional works at: https://scholarsarchive.byu.edu/etd Part of the Biology Commons BYU ScholarsArchive Citation Ebbert, Mark T., "Role of Epistasis in Alzheimer's Disease Genetics" (2014). Theses and Dissertations. 4325. https://scholarsarchive.byu.edu/etd/4325 This Dissertation is brought to you for free and open access by BYU ScholarsArchive. It has been accepted for inclusion in Theses and Dissertations by an authorized administrator of BYU ScholarsArchive. For more information, please contact [email protected], [email protected]. TIT L E PA G E Role of Epistasis in Alzheimer’s Disease Genetics Mark T. W. Ebbert A dissertation submitted to the faculty of Brigham Young University in partial fulfillment of the requirements for the degree of Doctor of Philosophy John S. K. Kauwe, Chair Perry G. Ridge Seth M. Bybee Mark J. Clement Chris D. Corcoran Stephen R. Piccolo Department of Biology Brigham Young University December 2014 Copyright © 2014 Mark T. W. Ebbert All Rights Reserved ABSTRACT Role of Epistasis in Alzheimer’s Disease Genetics Mark T. W. Ebbert Department of Biology, BYU Doctor of Philosophy Alzheimer’s disease is a complex neurodegenerative disease whose basic etiology and genetic structure remains elusive, despite decades of intensive investigation. To date, the significant genetic markers identified have no obvious functional effects, and are unlikely to play a role in Alzheimer’s disease etiology, themselves. These markers are likely linked to other genetic variations, rare or common.
    [Show full text]
  • Program in Human Neutrophils Fails To
    Downloaded from http://www.jimmunol.org/ by guest on September 25, 2021 is online at: average * The Journal of Immunology Anaplasma phagocytophilum , 20 of which you can access for free at: 2005; 174:6364-6372; ; from submission to initial decision 4 weeks from acceptance to publication J Immunol doi: 10.4049/jimmunol.174.10.6364 http://www.jimmunol.org/content/174/10/6364 Insights into Pathogen Immune Evasion Mechanisms: Fails to Induce an Apoptosis Differentiation Program in Human Neutrophils Dori L. Borjesson, Scott D. Kobayashi, Adeline R. Whitney, Jovanka M. Voyich, Cynthia M. Argue and Frank R. DeLeo cites 28 articles Submit online. Every submission reviewed by practicing scientists ? is published twice each month by Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts http://jimmunol.org/subscription Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html http://www.jimmunol.org/content/suppl/2005/05/03/174.10.6364.DC1 This article http://www.jimmunol.org/content/174/10/6364.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 © 2005 by The American Association of Immunologists All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. This information is current as of September 25, 2021. The Journal of Immunology Insights into Pathogen Immune Evasion Mechanisms: Anaplasma phagocytophilum Fails to Induce an Apoptosis Differentiation Program in Human Neutrophils1 Dori L.
    [Show full text]