A Meta-Analysis of Public Microarray Data Identifies Gene Regulatory
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Data Sheet Huil36g (152 A.A.)
Growth Factor Data Sheet GoldBio growth factors are manufactured for RESEARCH USE ONLY and cannot be sold for human consumption! Interleukin-36G (IL36G) is a pro-inflammatory cytokine that plays an important role in the pathophysiology of several diseases. IL36A, IL36B and IL36G (formerly IL1F6, IL1F8, and IL1F9) are IL1 family members that signal through the IL1 receptor family members IL1Rrp2 (IL1RL2) and IL1RAcP. IL36G is secreted when transfected into 293-T cells and could constitute part of an independent signaling system analogous to that of IL1A and IL1B receptor agonist and interleukin-1 receptor type I (IL1R1). Furthermore, IL36G also can function as an agonist of NFκB activation through the orphan IL1- receptor-related protein 2. Human IL36G (152 a.a.) shares 58%, 59%, 68% and 69% amino acid sequence identity with mouse, rat, bovine and equine IL36G, respectively, and 23-57% amino acid sequence identity with other family members. Catalog Number 1110-36F Product Name IL36G (IL-36 gamma), Human (152 a.a.) Recombinant Human Interleukin-36γ IL36G, IL36γ Interleukin 1 Homolog 1 (IL1H1) Interleukin 1-Related Protein 2 (IL1RP2) Interleukin 1 Family, Member 9 (IL1F9) Source Escherichia coli MW ~17.0 kDa (152 amino acids) Sequence SMCKPITGTI NDLNQQVWTL QGQNLVAVPR SDSVTPVTVA VITCKYPEAL EQGRGDPIYL GIQNPEMCLY CEKVGEQPTL QLKEQKIMDL YGQPEPVKPF LFYRAKTGRT STLESVAFPD WFIASSKRDQ PIILTSELGK SYNTAFELNI ND Accession Number Q9NZH8 Purity >95% by SDS-PAGE and HPLC analyses Biological Activity Fully biologically active when compared to standard. The ED50 as determined by its ability to induce IL-8 secretion by human preadipocytes is less than 10 ng/ml, corresponding to a specific activity of >1 × 105 IU/mg. -
Huil36g 169 Data Sheet
Growth Factor Data Sheet GoldBio growth factors are manufactured for RESEARCH USE ONLY and cannot be sold for human consumption! Interleukin-36G (IL36G) is a pro-inflammatory cytokine that plays an important role in the pathophysiology of several diseases. IL36A, IL36B and IL36G; (formerly IL1F6, IL1F8, and IL1F9) are IL1 family members that signal through the IL1 receptor family members IL1Rrp2 (IL1RL2) and IL1RAcP. IL36B is secreted when transfected into 293-T cells and could constitute part of an independent signaling system analogous to that of IL1A and IL1B receptor agonist and interleukin-1 receptor type I (IL1R1). Furthermore, IL36G also can function as an agonist of NFκB activation through the orphan IL1- receptor-related protein 2. Recombinant human IL36G is synthesized as a protein that contains no signal sequence, no prosegment and no potential N-linked glycosylation site.There is a 53% amino acid homology between human and mouse IL36G. IL36G also has a 25-55% amino acid homology with IL36G and IL1RN, IL1B, IL36RN, IL36A, IL37, IL36B and IL1F10. Catalog Number 1110-36E Product Name IL36G (IL-36 gamma), Human (169 a.a.) Recombinant Human Interleukin-36γ IL36G, IL36γ Interleukin 1 Homolog 1 (IL1H1) Interleukin 1-Related Protein 2 (IL1RP2) Interleukin 1 Family, Member 9 (IL1F9) Source Escherichia coli MW 18.7 kDa (169 amino acids) Sequence MRGTPGDADG GGRAVYQSMC KPITGTINDL NQQVWTLQGQ NLVAVPRSDS VTPVTVAVIT CKYPEALEQG RGDPIYLGIQ NPEMCLYCEK VGEQPTLQLK EQKIMDLYGQ PEPVKPFLFY RAKTGRTSTL ESVAFPDWFI ASSKRDQPII LTSELGKSYN TAFELNIND Accession Number Q9NZH8 Purity >95% by SDS-PAGE and HPLC analyses Biological Activity Fully biologically active when compared to standard. The specific activity is determined by its binding ability in a functional ELISA. -
Association of an Interleukin 1B Gene Polymorphism (-511) With
400 LETTER TO JMG Association of an interleukin 1B gene polymorphism (−511) with Parkinson’s disease in Finnish patients K M Mattila, J O Rinne, T Lehtimäki, M Röyttä, J-P Ahonen, M Hurme ............................................................................................................................. J Med Genet 2002;39:400–402 lzheimer’s disease (AD) and Parkinson’s disease (PD) are the two most common neurodegenerative conditions Table 1 Genotype and allele frequencies of the IL1 characterised by the presence of abnormal accumula- gene cluster polymorphisms in AD, PD, and control A patients tion of proteins and loss of neurones in specific regions of the brain. The aetiology and pathogenesis of AD and PD still Controls remain largely unknown. Evidence has emerged that immune Polymorphism AD (n=92) PD (n=52) (n=73) mediated mechanisms may be important in the development − 12 IL1A ( 889) of these disorders, and cytokine interleukin 1 (IL1) is one of *1/*1 42 (0.46) 28 (0.54) 33 (0.45) the mediators suggested to be involved. *1/*2 39 (0.42) 20 (0.38) 29 (0.40) The IL1 family comprises three proteins, the proinflamma- *2/*2 11 (0.12) 4 (0.08) 11 (0.15) tory IL1α and IL1β and their inhibitor IL1 receptor antagonist *1 123 (0.67) 76 (0.73) 95 (0.65) *2 61 (0.32) 28 (0.27) 51 (0.35) (IL1Ra), which are encoded by the IL1A, IL1B, and IL1RN − genes respectively.3 Since IL1 may have a role in AD4–8 and in IL1B ( 511) 910 *1/*1 35 (0.38) 25 (0.48) 24 (0.32) PD, variation in the IL1A, IL1B, and IL1RN genes may be of *1/*2 47 (0.51) 25 (0.48) 30 (0.41) importance in the development of these disorders. -
Genetic Determinants of Circulating Interleukin-1 Receptor Antagonist Levels and Their Association with Glycemic Traits
View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Trepo - Institutional Repository of Tampere University GENETIC DETERMINANTS OF CIRCULATING INTERLEUKIN-1 RECEPTOR ANTAGONIST LEVELS AND THEIR ASSOCIATION WITH GLYCEMIC TRAITS Marja-Liisa Nuotio Syventävien opintojen kirjallinen työ Tampereen yliopisto Lääketieteen yksikkö Tammikuu 2015 Tampereen yliopisto Lääketieteen yksikkö NUOTIO MARJA-LIISA: GENETIC DETERMINANTS OF CIRCULATING INTERLEUKIN-1 RECEPTOR ANTAGONIST LEVELS AND THEIR ASSOCIATION WITH GLYCEMIC TRAITS Kirjallinen työ, 57 s. Ohjaaja: professori Mika Kähönen Tammikuu 2015 Avainsanat: sytokiinit, insuliiniresistenssi, tyypin 2 diabetes, tulehdus, glukoosimetabolia, genominlaajuinen assosiaatioanalyysi (GWAS) Tulehdusta välittäviin sytokiineihin kuuluvan interleukiini 1β (IL-1β):n kohonneen systeemisen pitoisuuden on arveltu edesauttavan insuliiniresistenssin kehittymistä ja johtavan haiman β-solujen toimintahäiriöihin. IL-1β:n sisäsyntyisellä vastavaikuttajalla, interleukiini 1 reseptoriantagonistilla (IL-1RA), on puolestaan esitetty olevan suojaava rooli mainittujen fenotyyppien kehittymisessä päinvastaisten vaikutustensa ansiosta. IL-1RA:n suojaavan roolin havainnollistamiseksi työssä Genetic determinants of circulating interleukin-1 receptor antagonist levels and their association with glycemic traits tunnistettiin veren IL-1RA- pitoisuuteen assosioituvia geneettisiä variantteja, minkä jälkeen selvitettiin näiden yhteyttä glukoosi- ja insuliinimetaboliaan liittyvien muuttujien-, sekä -
Transcriptional Repression of IFN Regulatory Factor 7 by MYC Is Critical for Type I IFN Production in Human Plasmacytoid Dendrit
Transcriptional Repression of IFN Regulatory Factor 7 by MYC Is Critical for Type I IFN Production in Human Plasmacytoid Dendritic Cells This information is current as of September 28, 2021. Tae Whan Kim, Seunghee Hong, Yin Lin, Elise Murat, HyeMee Joo, Taeil Kim, Virginia Pascual and Yong-Jun Liu J Immunol 2016; 197:3348-3359; Prepublished online 14 September 2016; doi: 10.4049/jimmunol.1502385 Downloaded from http://www.jimmunol.org/content/197/8/3348 Supplementary http://www.jimmunol.org/content/suppl/2016/09/14/jimmunol.150238 http://www.jimmunol.org/ Material 5.DCSupplemental References This article cites 74 articles, 25 of which you can access for free at: http://www.jimmunol.org/content/197/8/3348.full#ref-list-1 Why The JI? Submit online. • Rapid Reviews! 30 days* from submission to initial decision by guest on September 28, 2021 • 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 © 2016 by The American Association of Immunologists, Inc. All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. The Journal of Immunology Transcriptional Repression of IFN Regulatory Factor 7 by MYC Is Critical for Type I IFN Production in Human Plasmacytoid Dendritic Cells Tae Whan Kim,*,1 Seunghee Hong,*,1 Yin Lin,* Elise Murat,* HyeMee Joo,* Taeil Kim,†,2 Virginia Pascual,* and Yong-Jun Liu*,† Type I IFNs are crucial mediators of human innate and adaptive immunity and are massively produced from plasmacytoid dendritic cells (pDCs). -
Interferon-Α Therapy in Bcr-Abl-Negative Myeloproliferative Neoplasms
Leukemia (2008) 22, 1990–1998 & 2008 Macmillan Publishers Limited All rights reserved 0887-6924/08 $32.00 www.nature.com/leu SPOTLIGHT REVIEW Interferon-a therapy in bcr-abl-negative myeloproliferative neoplasms J-J Kiladjian1,2,3, C Chomienne4 and P Fenaux1 1Assistance PubliqueFHoˆpitaux de Paris, Hoˆpital Avicenne, Service d’He´matologie Clinique, Bobigny, France; 2Assistance PubliqueFHoˆpitaux de Paris, Hoˆpital Saint-Louis, Centre d’Investigation Clinique, Paris, France; 3Universite´ Paris 7, Denis Diderot, Paris, France and 4Assistance PubliqueFHoˆpitaux de Paris, Hoˆpital Saint-Louis, Unite´ de Biologie Cellulaire, Paris, France Interferon (IFN) was the first cytokine discovered 50 years ago, however, did not allow complete purity, and although leukocyte with a wide range of biological properties, including immuno- IFN consisted predominantly of IFN-a, small amounts of other modulatory, proapoptotic and antiangiogenic activities, that rapidly raised interest in its therapeutic use in malignancies. IFN species were also present. Later on, the cloning of IFN-receptor characterization was also pivotal in the discovery recombinant human IFN-a and -b in 1980 allowed the SPOTLIGHT of the JAK/STAT signaling pathway. Among the large IFN production of large amounts of IFN for characterization, family, mainly one of the type I IFN, IFN-a2, is used in therapy. biological activity studies and clinical trials.5–7 It is only 20 Many clinical trials have shown remarkable efficacy of IFN-a in years after their discovery that two IFN species, IFN-a and -b, bcr-abl-negative myeloproliferative neoplasms (MPNs), espe- could be purified satisfactorily using high-performance liquid cially polycythemia vera (PV), and essential thrombocythemia 8 (ET). -
IL36G Blocking Peptide (CDBP5559) This Product Is for Research Use Only and Is Not Intended for Diagnostic Use
IL36G blocking peptide (CDBP5559) This product is for research use only and is not intended for diagnostic use. PRODUCT INFORMATION Antigen Description The protein encoded by this gene is a member of the interleukin 1 cytokine family. The activity of this cytokine is mediated by interleukin 1 receptor-like 2 (IL1RL2/IL1R-rp2), and is specifically inhibited by interleukin 1 family, member 5 (IL1F5/IL-1 delta). Interferon-gamma, tumor necrosis factor-alpha and interleukin 1, beta (IL1B) are reported to stimulate the expression of this cytokine in keratinocytes. The expression of this cytokine in keratinocytes can also be induced by a contact hypersensitivity reaction or herpes simplex virus infection. This gene and eight other interleukin 1 family genes form a cytokine gene cluster on chromosome 2. Two alternatively spliced transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Jun 2013] Immunogen 13 amino acids near the carboxy terminus of human IL-36G. Nature Synthetic Expression System N/A Species Reactivity Human Conjugate Unconjugated Applications Used as a blocking peptide in immunoblotting applications. Procedure None Format Liquid Concentration 200 μg/mL Size 0.05mg Preservative None Storage -20°C ANTIGEN GENE INFORMATION Gene Name IL36G interleukin 36, gamma [ Homo sapiens (human) ] Official Symbol IL36G 45-1 Ramsey Road, Shirley, NY 11967, USA Email: [email protected] Tel: 1-631-624-4882 Fax: 1-631-938-8221 1 © Creative Diagnostics All Rights Reserved Synonyms IL36G; interleukin -
Comprehensive Association Study of Genetic Variants in the IL-1 Gene Family in Systemic Juvenile Idiopathic Arthritis
Genes and Immunity (2008) 9, 349–357 & 2008 Nature Publishing Group All rights reserved 1466-4879/08 $30.00 www.nature.com/gene ORIGINAL ARTICLE Comprehensive association study of genetic variants in the IL-1 gene family in systemic juvenile idiopathic arthritis CJW Stock1, EM Ogilvie1, JM Samuel1, M Fife1, CM Lewis2 and P Woo1 1Centre for Paediatric and Adolescent Rheumatology, Windeyer Institute for Medical Sciences, University College London, London, UK and 2Guy’s, Kings and St Thomas’ School of Medicine, London, UK Patients with systemic juvenile idiopathic arthritis (sJIA) have a characteristic daily spiking fever and elevated levels of inflammatory cytokines. Members of the interleukin-1 (IL-1) gene family have been implicated in various inflammatory and autoimmune diseases, and treatment with the IL-1 receptor antagonist, Anakinra, shows remarkable improvement in some patients. This work describes the most comprehensive investigation to date of the involvement of the IL-1 gene family in sJIA. A two-stage case–control association study was performed to investigate the two clusters of IL-1 family genes using a tagging single nucleotide polymorphism (SNP) approach. Genotyping data of 130 sJIA patients and 151 controls from stage 1 highlighted eight SNPs in the IL1 ligand cluster region and two SNPs in the IL1 receptor cluster region as showing a significant frequency difference between the populations. These 10 SNPs were typed in an additional 105 sJIA patients and 184 controls in stage 2. Meta-analysis of the genotypes from both stages showed that three IL1 ligand cluster SNPs (rs6712572, rs2071374 and rs1688075) and one IL1 receptor cluster SNP (rs12712122) show evidence of significant association with sJIA. -
Type I Interferons in Anticancer Immunity
REVIEWS Type I interferons in anticancer immunity Laurence Zitvogel1–4*, Lorenzo Galluzzi1,5–8*, Oliver Kepp5–9, Mark J. Smyth10,11 and Guido Kroemer5–9,12 Abstract | Type I interferons (IFNs) are known for their key role in antiviral immune responses. In this Review, we discuss accumulating evidence indicating that type I IFNs produced by malignant cells or tumour-infiltrating dendritic cells also control the autocrine or paracrine circuits that underlie cancer immunosurveillance. Many conventional chemotherapeutics, targeted anticancer agents, immunological adjuvants and oncolytic 1Gustave Roussy Cancer Campus, F-94800 Villejuif, viruses are only fully efficient in the presence of intact type I IFN signalling. Moreover, the France. intratumoural expression levels of type I IFNs or of IFN-stimulated genes correlate with 2INSERM, U1015, F-94800 Villejuif, France. favourable disease outcome in several cohorts of patients with cancer. Finally, new 3Université Paris Sud/Paris XI, anticancer immunotherapies are being developed that are based on recombinant type I IFNs, Faculté de Médecine, F-94270 Le Kremlin Bicêtre, France. type I IFN-encoding vectors and type I IFN-expressing cells. 4Center of Clinical Investigations in Biotherapies of Cancer (CICBT) 507, F-94800 Villejuif, France. Type I interferons (IFNs) were first discovered more than Type I IFNs in cancer immunosurveillance 5Equipe 11 labellisée par la half a century ago as the factors underlying viral inter Type I IFNs are known to mediate antineoplastic effects Ligue Nationale contre le ference — that is, the ability of a primary viral infection against several malignancies, which is a clinically rel Cancer, Centre de Recherche 1 des Cordeliers, F-75006 Paris, to render cells resistant to a second distinct virus . -
Heatmaps - the Gene Expression Edition
Heatmaps - the gene expression edition Jeff Oliver 20 July, 2020 An application of heatmap visualization to investigate differential gene expression. Learning objectives 1. Manipulate data into a ‘tidy’ format 2. Visualize data in a heatmap 3. Become familiar with ggplot syntax for customizing plots Heatmaps for differential gene expression Heatmaps are a great way of displaying three-dimensional data in only two dimensions. But how can we easily translate tabular data into a format for heatmap plotting? By taking advantage of “data munging” and graphics packages, heatmaps are relatively easy to produce in R. Getting started We are going to start by isolating different types of information by imposing structure in our file managment. That is, we are going to put our input data in one folder and any output such as plots or analytical results in a different folder. We can use the dir.create to create these two folders: dir.create("data") dir.create("output") For this lesson, we will use a subset of data on a study of gene expression in cells infected with the influenza virus (doi: 10.4049/jimmunol.1501557). The study infected human plasmacytoid dendritic cells with the influenza virus, and compared gene expression in those cells to gene expression in uninfected cells. Thegoal was to see how the flu virus affected the function of these immune system cells. The data for this lesson is available at: http://tinyurl.com/flu-expression-data or https://jcoliver.github.io/ learn-r/data/GSE68849-expression.csv. Download this comma separated file and put it in the data folder. -
Evolutionary Divergence and Functions of the Human Interleukin (IL) Gene Family Chad Brocker,1 David Thompson,2 Akiko Matsumoto,1 Daniel W
UPDATE ON GENE COMPLETIONS AND ANNOTATIONS Evolutionary divergence and functions of the human interleukin (IL) gene family Chad Brocker,1 David Thompson,2 Akiko Matsumoto,1 Daniel W. Nebert3* and Vasilis Vasiliou1 1Molecular Toxicology and Environmental Health Sciences Program, Department of Pharmaceutical Sciences, University of Colorado Denver, Aurora, CO 80045, USA 2Department of Clinical Pharmacy, University of Colorado Denver, Aurora, CO 80045, USA 3Department of Environmental Health and Center for Environmental Genetics (CEG), University of Cincinnati Medical Center, Cincinnati, OH 45267–0056, USA *Correspondence to: Tel: þ1 513 821 4664; Fax: þ1 513 558 0925; E-mail: [email protected]; [email protected] Date received (in revised form): 22nd September 2010 Abstract Cytokines play a very important role in nearly all aspects of inflammation and immunity. The term ‘interleukin’ (IL) has been used to describe a group of cytokines with complex immunomodulatory functions — including cell proliferation, maturation, migration and adhesion. These cytokines also play an important role in immune cell differentiation and activation. Determining the exact function of a particular cytokine is complicated by the influence of the producing cell type, the responding cell type and the phase of the immune response. ILs can also have pro- and anti-inflammatory effects, further complicating their characterisation. These molecules are under constant pressure to evolve due to continual competition between the host’s immune system and infecting organisms; as such, ILs have undergone significant evolution. This has resulted in little amino acid conservation between orthologous proteins, which further complicates the gene family organisation. Within the literature there are a number of overlapping nomenclature and classification systems derived from biological function, receptor-binding properties and originating cell type. -
Np63 Regulates IL-33 and IL-31 Signaling in Atopic Dermatitis
Cell Death and Differentiation (2016) 23, 1073–1085 OPEN & 2016 Macmillan Publishers Limited All rights reserved 1350-9047/16 www.nature.com/cdd ΔNp63 regulates IL-33 and IL-31 signaling in atopic dermatitis JM Rizzo1,2, A Oyelakin3, S Min3, K Smalley1, J Bard1, W Luo1,7, J Nyquist4, E Guttman-Yassky5, T Yoshida6, A De Benedetto6, LA Beck6, S Sinha*,1 and R-A Romano*,3 Atopic dermatitis (AD) is the most common inflammatory skin disease with no well-delineated cause or effective cure. Here we show that the p53 family member p63, specifically the ΔNp63, isoform has a key role in driving keratinocyte activation in AD. We find that overexpression of ΔNp63 in transgenic mouse epidermis results in a severe skin phenotype that shares many of the key clinical, histological and molecular features associated with human AD. This includes pruritus, epidermal hyperplasia, aberrant keratinocyte differentiation, enhanced expression of selected cytokines and chemokines and the infiltration of large numbers of inflammatory cells including type 2 T-helper cells – features that are highly representative of AD dermatopathology. We further demonstrate several of these mediators to be direct transcriptional targets of ΔNp63 in keratinocytes. Of particular significance are two p63 target genes, IL-31 and IL-33, both of which are key players in the signaling pathways implicated in AD. Importantly, we find these observations to be in good agreement with elevated levels of ΔNp63 in skin lesions of human patients with AD. Our studies reveal an important role for ΔNp63 in the pathogenesis of AD and offer new insights into its etiology and possible therapeutic targets.