Mouse P2rx6 Conditional Knockout Project (CRISPR/Cas9)
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Cells Δγ Lineage Choice and Shapes Peripheral Purinergic P2X7
Purinergic P2X7 Receptor Drives T Cell Lineage Choice and Shapes Peripheral δγ Cells This information is current as Michela Frascoli, Jessica Marcandalli, Ursula Schenk and of October 2, 2021. Fabio Grassi J Immunol 2012; 189:174-180; Prepublished online 30 May 2012; doi: 10.4049/jimmunol.1101582 http://www.jimmunol.org/content/189/1/174 Downloaded from Supplementary http://www.jimmunol.org/content/suppl/2012/05/30/jimmunol.110158 Material 2.DC1 http://www.jimmunol.org/ References This article cites 31 articles, 15 of which you can access for free at: http://www.jimmunol.org/content/189/1/174.full#ref-list-1 Why The JI? Submit online. • Rapid Reviews! 30 days* from submission to initial decision • No Triage! Every submission reviewed by practicing scientists by guest on October 2, 2021 • 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 © 2012 by The American Association of Immunologists, Inc. All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. The Journal of Immunology Purinergic P2X7 Receptor Drives T Cell Lineage Choice and Shapes Peripheral gd Cells Michela Frascoli,* Jessica Marcandalli,* Ursula Schenk,*,1 and Fabio Grassi*,† TCR signal strength instructs ab versus gd lineage decision in immature T cells. -
Cellular and Molecular Signatures in the Disease Tissue of Early
Cellular and Molecular Signatures in the Disease Tissue of Early Rheumatoid Arthritis Stratify Clinical Response to csDMARD-Therapy and Predict Radiographic Progression Frances Humby1,* Myles Lewis1,* Nandhini Ramamoorthi2, Jason Hackney3, Michael Barnes1, Michele Bombardieri1, Francesca Setiadi2, Stephen Kelly1, Fabiola Bene1, Maria di Cicco1, Sudeh Riahi1, Vidalba Rocher-Ros1, Nora Ng1, Ilias Lazorou1, Rebecca E. Hands1, Desiree van der Heijde4, Robert Landewé5, Annette van der Helm-van Mil4, Alberto Cauli6, Iain B. McInnes7, Christopher D. Buckley8, Ernest Choy9, Peter Taylor10, Michael J. Townsend2 & Costantino Pitzalis1 1Centre for Experimental Medicine and Rheumatology, William Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, Charterhouse Square, London EC1M 6BQ, UK. Departments of 2Biomarker Discovery OMNI, 3Bioinformatics and Computational Biology, Genentech Research and Early Development, South San Francisco, California 94080 USA 4Department of Rheumatology, Leiden University Medical Center, The Netherlands 5Department of Clinical Immunology & Rheumatology, Amsterdam Rheumatology & Immunology Center, Amsterdam, The Netherlands 6Rheumatology Unit, Department of Medical Sciences, Policlinico of the University of Cagliari, Cagliari, Italy 7Institute of Infection, Immunity and Inflammation, University of Glasgow, Glasgow G12 8TA, UK 8Rheumatology Research Group, Institute of Inflammation and Ageing (IIA), University of Birmingham, Birmingham B15 2WB, UK 9Institute of -
Supplementary Table S4. FGA Co-Expressed Gene List in LUAD
Supplementary Table S4. FGA co-expressed gene list in LUAD tumors Symbol R Locus Description FGG 0.919 4q28 fibrinogen gamma chain FGL1 0.635 8p22 fibrinogen-like 1 SLC7A2 0.536 8p22 solute carrier family 7 (cationic amino acid transporter, y+ system), member 2 DUSP4 0.521 8p12-p11 dual specificity phosphatase 4 HAL 0.51 12q22-q24.1histidine ammonia-lyase PDE4D 0.499 5q12 phosphodiesterase 4D, cAMP-specific FURIN 0.497 15q26.1 furin (paired basic amino acid cleaving enzyme) CPS1 0.49 2q35 carbamoyl-phosphate synthase 1, mitochondrial TESC 0.478 12q24.22 tescalcin INHA 0.465 2q35 inhibin, alpha S100P 0.461 4p16 S100 calcium binding protein P VPS37A 0.447 8p22 vacuolar protein sorting 37 homolog A (S. cerevisiae) SLC16A14 0.447 2q36.3 solute carrier family 16, member 14 PPARGC1A 0.443 4p15.1 peroxisome proliferator-activated receptor gamma, coactivator 1 alpha SIK1 0.435 21q22.3 salt-inducible kinase 1 IRS2 0.434 13q34 insulin receptor substrate 2 RND1 0.433 12q12 Rho family GTPase 1 HGD 0.433 3q13.33 homogentisate 1,2-dioxygenase PTP4A1 0.432 6q12 protein tyrosine phosphatase type IVA, member 1 C8orf4 0.428 8p11.2 chromosome 8 open reading frame 4 DDC 0.427 7p12.2 dopa decarboxylase (aromatic L-amino acid decarboxylase) TACC2 0.427 10q26 transforming, acidic coiled-coil containing protein 2 MUC13 0.422 3q21.2 mucin 13, cell surface associated C5 0.412 9q33-q34 complement component 5 NR4A2 0.412 2q22-q23 nuclear receptor subfamily 4, group A, member 2 EYS 0.411 6q12 eyes shut homolog (Drosophila) GPX2 0.406 14q24.1 glutathione peroxidase -
Ion Channels
UC Davis UC Davis Previously Published Works Title THE CONCISE GUIDE TO PHARMACOLOGY 2019/20: Ion channels. Permalink https://escholarship.org/uc/item/1442g5hg Journal British journal of pharmacology, 176 Suppl 1(S1) ISSN 0007-1188 Authors Alexander, Stephen PH Mathie, Alistair Peters, John A et al. Publication Date 2019-12-01 DOI 10.1111/bph.14749 License https://creativecommons.org/licenses/by/4.0/ 4.0 Peer reviewed eScholarship.org Powered by the California Digital Library University of California S.P.H. Alexander et al. The Concise Guide to PHARMACOLOGY 2019/20: Ion channels. British Journal of Pharmacology (2019) 176, S142–S228 THE CONCISE GUIDE TO PHARMACOLOGY 2019/20: Ion channels Stephen PH Alexander1 , Alistair Mathie2 ,JohnAPeters3 , Emma L Veale2 , Jörg Striessnig4 , Eamonn Kelly5, Jane F Armstrong6 , Elena Faccenda6 ,SimonDHarding6 ,AdamJPawson6 , Joanna L Sharman6 , Christopher Southan6 , Jamie A Davies6 and CGTP Collaborators 1School of Life Sciences, University of Nottingham Medical School, Nottingham, NG7 2UH, UK 2Medway School of Pharmacy, The Universities of Greenwich and Kent at Medway, Anson Building, Central Avenue, Chatham Maritime, Chatham, Kent, ME4 4TB, UK 3Neuroscience Division, Medical Education Institute, Ninewells Hospital and Medical School, University of Dundee, Dundee, DD1 9SY, UK 4Pharmacology and Toxicology, Institute of Pharmacy, University of Innsbruck, A-6020 Innsbruck, Austria 5School of Physiology, Pharmacology and Neuroscience, University of Bristol, Bristol, BS8 1TD, UK 6Centre for Discovery Brain Science, University of Edinburgh, Edinburgh, EH8 9XD, UK Abstract The Concise Guide to PHARMACOLOGY 2019/20 is the fourth in this series of biennial publications. The Concise Guide provides concise overviews of the key properties of nearly 1800 human drug targets with an emphasis on selective pharmacology (where available), plus links to the open access knowledgebase source of drug targets and their ligands (www.guidetopharmacology.org), which provides more detailed views of target and ligand properties. -
Polyhexamethylene Guanidine Phosphate Damages Tight Junctions and the F-Actin Architecture by Activating Calpain-1 Via the P2RX7/Ca2+ Signaling Pathway
cells Article Polyhexamethylene Guanidine Phosphate Damages Tight Junctions and the F-Actin Architecture by Activating Calpain-1 via the P2RX7/Ca2+ Signaling Pathway Sun Woo Jin y, Gi Ho Lee y, Hoa Thi Pham, Jae Ho Choi and Hye Gwang Jeong * College of Pharmacy, Chungnam National University, Daejeon 34134, Korea; [email protected] (S.W.J.); [email protected] (G.H.L.); [email protected] (H.T.P.); [email protected] (J.H.C.) * Correspondence: [email protected]; Tel.: +82-42-821-5936 These authors contributed equally to this work. y Received: 14 November 2019; Accepted: 22 December 2019; Published: 24 December 2019 Abstract: Polyhexamethylene guanidine phosphate (PHMG-p), a member of the polymeric guanidine family, has strong antimicrobial activity and may increase the risk of inflammation-associated pulmonary fibrosis. However, the effect of PHMG-p on the barrier function of the bronchial epithelium is unknown. Epithelial barrier functioning is maintained by tight junctions (TJs); damage to these TJs is the major cause of epithelial barrier breakdown during lung inflammation. The present study showed that, in BEAS-2B human bronchial epithelial cells, exposure to PHMG-p reduced the number of TJs and the E-cadherin level and impaired the integrity of the F-actin architecture. Furthermore, exposure to PHMG-p stimulated the calcium-dependent protease calpain-1, which breaks down TJs. However, treatment with the calpain-1 inhibitor, ALLN, reversed the PHMG-p-mediated impairment of TJs and the F-actin architecture. Furthermore, exposure to PHMG-p increased the intracellular Ca2+ level via P2X purinoreceptor 7 (P2RX7) and inhibition of P2RX7 abolished the PHMG-p-induced calpain-1 activity and protein degradation and increased the intracellular Ca2+ level. -
Genomics of Inherited Bone Marrow Failure and Myelodysplasia Michael
Genomics of inherited bone marrow failure and myelodysplasia Michael Yu Zhang A dissertation submitted in partial fulfillment of the requirements for the degree of Doctor of Philosophy University of Washington 2015 Reading Committee: Mary-Claire King, Chair Akiko Shimamura Marshall Horwitz Program Authorized to Offer Degree: Molecular and Cellular Biology 1 ©Copyright 2015 Michael Yu Zhang 2 University of Washington ABSTRACT Genomics of inherited bone marrow failure and myelodysplasia Michael Yu Zhang Chair of the Supervisory Committee: Professor Mary-Claire King Department of Medicine (Medical Genetics) and Genome Sciences Bone marrow failure and myelodysplastic syndromes (BMF/MDS) are disorders of impaired blood cell production with increased leukemia risk. BMF/MDS may be acquired or inherited, a distinction critical for treatment selection. Currently, diagnosis of these inherited syndromes is based on clinical history, family history, and laboratory studies, which directs the ordering of genetic tests on a gene-by-gene basis. However, despite extensive clinical workup and serial genetic testing, many cases remain unexplained. We sought to define the genetic etiology and pathophysiology of unclassified bone marrow failure and myelodysplastic syndromes. First, to determine the extent to which patients remained undiagnosed due to atypical or cryptic presentations of known inherited BMF/MDS, we developed a massively-parallel, next- generation DNA sequencing assay to simultaneously screen for mutations in 85 BMF/MDS genes. Querying 71 pediatric and adult patients with unclassified BMF/MDS using this assay revealed 8 (11%) patients with constitutional, pathogenic mutations in GATA2 , RUNX1 , DKC1 , or LIG4 . All eight patients lacked classic features or laboratory findings for their syndromes. -
Novel Approach to Chronic Cough
Moksliniai darbai ir apžvalgos Novel approach to chronic cough NAUJAS POŽIŪRIS Į LĖTINĮ KOSULĮ LAIMA KONDRATAVIČIENĖ, KRISTINA BIEKŠIENĖ, SKAIDRIUS MILIAUSKAS Department of Pulmonology, Medical Academy, Lithuanian University of Health Sciences Summary. Cough is the most common symptom for which people seek medical advice. A multitude of reasons can cause it. In clinical practice, a new term “Cough hypersensitivity syndrome“ was proposed, which defines unaccountable reasons for cough and different groups of patients with chronic cough. Adenosine triphosphate (ATP) as a driver of chronic cough is the most important target in nowadays clinical trials. Extracellular ATP activates P2X purinoreceptor 3 (P2X3) receptor channels, which are expressed in sensory neurons. New treatment methods that block P2X3 receptors are being developed. Keywords: chronic cough, cough hypersensitivity syndrome, adenosine triphosphate, novel treatment options. Santrauka. Lėtinis kosulys yra dažniausias skundas, dėl kurio pacientai kreipiasi į gydytojus. Kosulį sukelia įvairios priežastys ir sutrikimai. Klinikinėje praktikoje vartojamas naujas terminas „Kosulio hiperjautrumo sindromas“, kuris apima neaiškos kilmės kosulio priežastis bei skirtingas pacientų, besiskundžiančių lėtiniu kosuliu, grupes. Adenozino trifosfatas (ATP), kaip vienas pagrindinių kosulį sukeliančių veiksnių, šiuo metu yra dažniausiai klinikiniuose tyrimuose tiriama cheminė medžiaga. ATP aktyvuoja P2X purino receptoriaus 3 (P2X3) jonų kanalus, kurie yra išreikšti jutiminiuose neuronuose. Nauji -
Datasheet BA3178 Anti-P2RX6 Antibody
Product datasheet Anti-P2RX6 Antibody Catalog Number: BA3178 BOSTER BIOLOGICAL TECHNOLOGY Special NO.1, International Enterprise Center, 2nd Guanshan Road, Wuhan, China Web: www.boster.com.cn Phone: +86 27 67845390 Fax: +86 27 67845390 Email: [email protected] Basic Information Product Name Anti-P2RX6 Antibody Gene Name P2RX6 Source Rabbit IgG Species Reactivity human Tested Application WB Contents 500ug/ml antibody with PBS ，0.02% NaN3 , 1mg BSA and 50% glycerol. Immunogen A synthetic peptide corresponding to a sequence at the C-terminus of human P2X6(387-406aa VWRELALASQARLAECLRRS). Purification Immunogen affinity purified. Observed MW 60KD Dilution Ratios Western blot: 1:500-2000 Storage 12 months from date of receipt，-20℃ as supplied.6 months 2 to 8℃ after reconstitution. Avoid repeated freezing and thawing Background Information Purinergic receptor P2X-Like 1, also known as P2X6, is a protein that in humans is encoded by the P2RX6 gene. The encoded protein is associated with VE-cadherin at the adherens junctions of human umbilical vein endothelial cells. This gene belongs to the family of P2X receptors. P2RXL1 gene was mapped to chromosome 22q11 by fluorescence in situ hybridization. This gene is a receptor for ATP that acts as a ligand-gated ion channel. It can mediate rapid and selective permeability to cations. Reference Anti-P2RX6 Antibody被引用在0文献中。 暂无引用 FOR RESEARCH USE ONLY. NOT FOR DIAGNOSTIC AND CLINICAL USE. 1 Product datasheet Anti-P2RX6 Antibody Catalog Number: BA3178 BOSTER BIOLOGICAL TECHNOLOGY Special NO.1, International Enterprise Center, 2nd Guanshan Road, Wuhan, China Web: www.boster.com.cn Phone: +86 27 67845390 Fax: +86 27 67845390 Email: [email protected] Selected Validation Data Lane 1: U87 Cell LysateLane 2: 22RV1 Cell LysateLane 3: JURKAT Cell LysateLane 4: HT1080 Cell Lysate FOR RESEARCH USE ONLY. -
Downloaded Per Proteome Cohort Via the Web- Site Links of Table 1, Also Providing Information on the Deposited Spectral Datasets
www.nature.com/scientificreports OPEN Assessment of a complete and classifed platelet proteome from genome‑wide transcripts of human platelets and megakaryocytes covering platelet functions Jingnan Huang1,2*, Frauke Swieringa1,2,9, Fiorella A. Solari2,9, Isabella Provenzale1, Luigi Grassi3, Ilaria De Simone1, Constance C. F. M. J. Baaten1,4, Rachel Cavill5, Albert Sickmann2,6,7,9, Mattia Frontini3,8,9 & Johan W. M. Heemskerk1,9* Novel platelet and megakaryocyte transcriptome analysis allows prediction of the full or theoretical proteome of a representative human platelet. Here, we integrated the established platelet proteomes from six cohorts of healthy subjects, encompassing 5.2 k proteins, with two novel genome‑wide transcriptomes (57.8 k mRNAs). For 14.8 k protein‑coding transcripts, we assigned the proteins to 21 UniProt‑based classes, based on their preferential intracellular localization and presumed function. This classifed transcriptome‑proteome profle of platelets revealed: (i) Absence of 37.2 k genome‑ wide transcripts. (ii) High quantitative similarity of platelet and megakaryocyte transcriptomes (R = 0.75) for 14.8 k protein‑coding genes, but not for 3.8 k RNA genes or 1.9 k pseudogenes (R = 0.43–0.54), suggesting redistribution of mRNAs upon platelet shedding from megakaryocytes. (iii) Copy numbers of 3.5 k proteins that were restricted in size by the corresponding transcript levels (iv) Near complete coverage of identifed proteins in the relevant transcriptome (log2fpkm > 0.20) except for plasma‑derived secretory proteins, pointing to adhesion and uptake of such proteins. (v) Underrepresentation in the identifed proteome of nuclear‑related, membrane and signaling proteins, as well proteins with low‑level transcripts. -
Sugar Causes Obesity and Metabolic Syndrome in Mice Independently of Sweet Taste
Am J Physiol Endocrinol Metab 319: E276–E290, 2020. First published June 23, 2020; doi:10.1152/ajpendo.00529.2019. RESEARCH ARTICLE Sugar causes obesity and metabolic syndrome in mice independently of sweet taste Ana Andres-Hernando,1 Masanari Kuwabara,1 X David J. Orlicky,2 Aurelie Vandenbeuch,3,4 Christina Cicerchi,1 Sue C. Kinnamon,3,4 Thomas E. Finger,4,5 X Richard J. Johnson,1 and X Miguel A. Lanaspa1 1Division of Renal Diseases and Hypertension, University of Colorado School of Medicine, University of Colorado, Aurora, Colorado; 2Department of Pathology, University of Colorado School of Medicine, University of Colorado, Aurora, Colorado; 3Department of Otolaryngology, University of Colorado School of Medicine, University of Colorado, Aurora, Colorado; 4Rocky Mountain Taste & Smell Center, University of Colorado School of Medicine, University of Colorado, Aurora, Colorado; and 5Department of Cell and Developmental Biology, University of Colorado School of Medicine, University of Colorado, Aurora, Colorado Submitted 5 December 2019; accepted in final form 16 June 2020 Andres-Hernando A, Kuwabara M, Orlicky DJ, Vandenbeuch caloric sweeteners has skyrocketed over the last several cen- A, Cicerchi C, Kinnamon SC, Finger TE, Johnson RJ, Lanaspa turies, from an intake (based on sales) of ~4 pounds per capita MA. Sugar causes obesity and metabolic syndrome in mice indepen- per year in 1700 to over 150 pounds per capita per year in 2000 dently of sweet taste. Am J Physiol Endocrinol Metab 319: E276– E290, 2020. First published June 23, 2020; doi:10.1152/ajpendo. (12). Today nearly 70% of processed foods and beverages in 00529.2019.—Intake of sugars, especially the fructose component, is US supermarkets contain these sweeteners, including many strongly associated with the development of obesity and metabolic foods that one might initially not consider to contain such syndrome, but the relative role of taste versus metabolism in driving additives (30). -
Ion Channels and Transporters in Lymphocyte Function and Immunity
REVIEWS Ion channels and transporters in lymphocyte function and immunity Stefan Feske1, Edward Y. Skolnik2 and Murali Prakriya3 Abstract | Lymphocyte function is regulated by a network of ion channels and transporters in the plasma membrane of B and T cells. These proteins modulate the cytoplasmic concentrations of diverse cations, such as calcium, magnesium and zinc ions, which function as second messengers to regulate crucial lymphocyte effector functions, including cytokine production, differentiation and cytotoxicity. The repertoire of ion-conducting proteins includes calcium release-activated calcium (CRAC) channels, P2X receptors, transient receptor potential (TRP) channels, potassium channels, chloride channels and magnesium and zinc transporters. This Review discusses the roles of ion conduction pathways in lymphocyte function and immunity. Ion channels and ion transporters function as gateways Store-operated calcium channels Ion channels 2+ Pore-forming transmembrane for charged ions that cannot freely diffuse across lipid Ca is a well-established second messenger in lympho proteins that enable the flow of membrane barriers. They regulate the intracellular cytes that regulates proliferation, gene expression, motil- ions down an electrochemical concentration of various ions, such as calcium (Ca2+), ity and other functions. Similarly to in other mammalian gradient. magnesium (Mg2+) and zinc (Zn2+). The movement of cell types, the intracellular Ca2+ concentration in unstim- Ion transporters these cations across the plasma membrane depends on ulated B and T cells is maintained at ~50–100 nM, which 4 2+ Pore-forming transmembrane electrical gradients that are maintained in turn by potas- is ~10 -fold lower than the Ca concentration in the proteins that carry ions sium (K+), sodium (Na+) and chloride (Cl−) channels. -
And Cystein Cathepsin-Dependent Cancer Cells Invasiveness
Oncogene (2011) 30, 2108–2122 & 2011 Macmillan Publishers Limited All rights reserved 0950-9232/11 www.nature.com/onc ORIGINAL ARTICLE P2X7 receptor activation enhances SK3 channels- and cystein cathepsin-dependent cancer cells invasiveness B Jelassi1, A Chantoˆme1, F Alcaraz-Pe´rez2, A Baroja-Mazo3, ML Cayuela2, P Pelegrin3,4, A Surprenant4 and S Roger1 1Inserm U921, Universite´ Franc¸ois Rabelais de Tours, 10 Boulevard Tonnelle´, Tours, France; 2Telomerase, Cancer and Aging Group, University Hospital ‘Virgen de la Arrixaca’-FFIS, Carretera Palmar, Murcia, Spain; 3Inflammation and Experimental Surgery Group, University Hospital ‘Virgen de la Arrixaca’-FFIS, Carretera Palmar, Murcia, Spain and 4Faculty of Life Science, Michael Smith Building D3315, University of Manchester, Manchester, UK ATP-gated P2X7 receptors (P2X7R) are unusual plasma cancer patients do not die because of local complications membrane ion channels that have been extensively studied of their primary solid tumour growth, which are in immune cells. More recently, P2X7R have been relatively well treated, but rather to the appearance of described as potential cancer cell biomarkers. However, metastases. The development of metastases consists of a mechanistic links between P2X7R and cancer cell complex series of events accomplished by tumour cells processes are unknown. Here, we show, in the highly after they acquire numerous abilities, one of which being aggressive human breast cancer cell line MDA-MB-435s, the acquisition of an invasive potency. This mainly lies that P2X7 receptor is highly expressed and fully into an enhanced migration and the ability to digest the functional. Its activation is responsible for the extension extracellular matrix (Gupta and Massague, 2006).