DOCSLIB.ORG

Gene Section Mini Review

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Gene Section Mini Review Atlas of Genetics and Cytogenetics in Oncology and Haematology OPEN ACCESS JOURNAL AT INIST-CNRS Gene Section Mini Review IL22RA1 (interleukin 22 receptor, alpha 1) Pascal Gelebart, Raymond Lai Department of Laboratory Medicine and Pathology, Cross Cancer Institute, University of Alberta, Edmonton, Alberta, Canada (PG, RL) Published in Atlas Database: February 2010 Online updated version : http://AtlasGeneticsOncology.org/Genes/IL22RA1ID44568ch1p36.html DOI: 10.4267/2042/44908 This work is licensed under a Creative Commons Attribution-Noncommercial-No Derivative Works 2.0 France Licence. © 2010 Atlas of Genetics and Cytogenetics in Oncology and Haematology nucleotides, encoding a protein of 594 amino acid Identity residues. Other names: CRF2-9, IL22R, IL22R1 Pseudogene HGNC (Hugo): IL22RA1 None. Location: 1p36.11 Protein DNA/RNA Description Description IL22RA1 is composed of 574 amino acid residues, and The gene spans a region of 23.3 kb including seven the predicted molecular weight of the immature protein exons. is 63 kDa. IL22RA1 protein is composed of six putative domains, including the signal peptide (residue Transcription 1 to 15), the extracellular domain (residue 16 to 228), One only transcript form containing 7 exons has been the transmembrane domain (residue 229 to 249), the described. cytoplasmic domain (residue 250 to 574), and two The last exon is partially untranslated. The transcript fibronectin type-III domains (residue 18-115 and 141- length is 1725 221). Representation of the IL22RA1 gene organization. IL22RA1 gene and RNA. Atlas Genet Cytogenet Oncol Haematol. 2010; 14(12) 1106 IL22RA1 (interleukin 22 receptor, alpha 1) Gelebart P, Lai R IL22RA1 protein organization and localization. IL22RA1 protein domains. Localization of IL22RA1 by immunufluorescence confocal microscopy in ALK+ALCL cells. Expression IL22RA1 expression is relatively restricted, being found at the highest level in the pancreas, small intestine, colon, kidney, and liver. Importantly, IL22RA1 is not detectable in normal immune cells, including monocytes, B-cells, T-cells, natural killer cells, macrophages and dendritic cells, cell types that are normally found in the bone marrow, peripheral blood, thymus and spleen. Localisation IL22RA1 is localized at the plasma membrane. Crystal structure of IL22RA1 with IL22 at 1.9 A resolution. Adapted from PDB (access number: 3DLQ). Atlas Genet Cytogenet Oncol Haematol. 2010; 14(12) 1107 IL22RA1 (interleukin 22 receptor, alpha 1) Gelebart P, Lai R FACS analysis of IL22RA1 expression in peripheral mononuclear cells from healthy donor. IL22RA1 signaling. Function and translocate to the nucleus to modulate the transcription of various target genes. IL22RA1 is one of the subunits of the IL20, IL22 and IL24 receptor complex. Cytokine binding to IL22RA1 results in its aggregation, which activates the associated Mutations JAK via its autophosphorylation. This in turn leads to Site-directed mutagenesis experiments have revealed the phosphorylation and activation of STAT proteins. critical amino acid residues involved in its binding to Subsequently, phosphorylated STAT proteins dimerize IL22. Specifically, mutation of residue 58 from K to A Atlas Genet Cytogenet Oncol Haematol. 2010; 14(12) 1108 IL22RA1 (interleukin 22 receptor, alpha 1) Gelebart P, Lai R reduces the binding of IL22. Mutation of the residue 60 the chromosomal translocation is that of the from Y to A or R results in a complete loss of response t(2;5)(p23;q35), which leads to the juxtaposition of the to IL22. nucleophosmin (NPM) gene at 5q35 with the ALK Natural IL22RA1 variants have been reported, gene at 2p23. Mounting evidence suggests that the including those carrying mutations at the residue 130 (S resulted oncogenic fusion protein, NPM-ALK, plays to P), 205 (V to I), 209 (A to S), 222 (L to P), 407 (M crucial roles in the pathogenesis of these tumors. to V) and 518 (R to G). Prognosis Patients with ALK+ALCL are typically treated with Implicated in combination chemotherapy containing doxorubicin. ALK-positive anaplastic large cell ALK+ALCL represents one of the most common pediatric lymphoid malignancies. The prognosis of lymphoma (ALK+ALCL) pediatric ALK+ALCL patients is significant better than that of adult patients. Disease Cytogenetics Anaplastic lymphoma kinase (ALK)-positive anaplastic t(2;5)(p23;q35) in most ALK+ALCL patients; other large-cell lymphoma (ALCL), or ALK+ALCL, is a translocation variants have been described. specific type of non-Hodgkin lymphoma characterized Hybrid/Mutated gene by the T/null-cell immunophenotype, consistent NPM-ALK expression of CD30 and reciprocal chromosomal translocations involving the ALK gene. In most cases, Representation of the NPM-ALK oncoprotein organization and sequence. Abnormal protein NPM-ALK References Kotenko SV, Izotova LS, Mirochnitchenko OV, Esterova E, Dickensheets H, Donnelly RP, Pestka S. Identification of the functional interleukin-22 (IL-22) receptor complex: the IL-10R2 chain (IL-10Rbeta ) is a common chain of both the IL-10 and IL-22 (IL-10-related T cell-derived inducible factor, IL-TIF) Structure of the oncogenic fusion protein NPM-ALK. receptor complexes. J Biol Chem. 2001 Jan 26;276(4):2725-32 Oncogenesis Lécart S, Morel F, Noraz N, Pène J, Garcia M, Boniface K, Aberrant expression of IL22RA1 in ALK+ALCL Lecron JC, Yssel H. IL-22, in contrast to IL-10, does not induce Ig production, due to absence of a functional IL-22 receptor on lymphoma cells allows these cells to be responsive to activated human B cells. Int Immunol. 2002 Nov;14(11):1351-6 IL-22 stimulation, which further stimulate STAT3 Wang M, Tan Z, Zhang R, Kotenko SV, Liang P. Interleukin 24 signaling and the growth of these cells. Blocking the (MDA-7/MOB-5) signals through two heterodimeric receptors, IL-22 signaling pathway using a neutralizing antibody IL-22R1/IL-20R2 and IL-20R1/IL-20R2. J Biol Chem. 2002 Mar has been shown to significantly decrease the growth of 1;277(9):7341-7 ALK+ALCL cells in-vitro. The aberrant expression of Dumoutier L, Lejeune D, Hor S, Fickenscher H, Renauld JC. IL22RA1 in ALK+ALCL is dependent on the Cloning of a new type II cytokine receptor activating signal expression of NPM-ALK, since siRNA to transducer and activator of transcription (STAT)1, STAT2 and downregulate NPM-ALK dramatically shut down STAT3. Biochem J. 2003 Mar 1;370(Pt 2):391-6 IL22RA1 expression. Amin HM, Lai R. Pathobiology of ALK+ anaplastic large-cell lymphoma. Blood. 2007 Oct 1;110(7):2259-67 Atlas Genet Cytogenet Oncol Haematol. 2010; 14(12) 1109 IL22RA1 (interleukin 22 receptor, alpha 1) Gelebart P, Lai R Bard JD, Gelebart P, Anand M, Amin HM, Lai R. Aberrant interleukin-22 receptor recruits STAT3 by interacting with its expression of IL-22 receptor 1 and autocrine IL-22 stimulation coiled-coil domain. J Biol Chem. 2009 Sep 25;284(39):26377- contribute to tumorigenicity in ALK+ anaplastic large cell 84 lymphoma. Leukemia. 2008 Aug;22(8):1595-603 Endam LM, Bossé Y, Filali-Mouhim A, Cormier C, Boisvert P, Bleicher L, de Moura PR, Watanabe L, Colau D, Dumoutier L, Boulet LP, Hudson TJ, Desrosiers M. Polymorphisms in the Renauld JC, Polikarpov I. Crystal structure of the IL-22/IL- interleukin-22 receptor alpha-1 gene are associated with 22R1 complex and its implications for the IL-22 signaling severe chronic rhinosinusitis. Otolaryngol Head Neck Surg. mechanism. FEBS Lett. 2008 Sep 3;582(20):2985-92 2009 May;140(5):741-7 de Oliveira Neto M, Ferreira JR Jr, Colau D, Fischer H, This article should be referenced as such: Nascimento AS, Craievich AF, Dumoutier L, Renauld JC, Polikarpov I. Interleukin-22 forms dimers that are recognized Gelebart P, Lai R. IL22RA1 (interleukin 22 receptor, alpha 1). by two interleukin-22R1 receptor chains. Biophys J. 2008 Mar Atlas Genet Cytogenet Oncol Haematol. 2010; 14(12):1106- 1;94(5):1754-65 1110. Dumoutier L, de Meester C, Tavernier J, Renauld JC. New activation modus of STAT3: a tyrosine-less region of the Atlas Genet Cytogenet Oncol Haematol. 2010; 14(12) 1110 .
Load more

Recommended publications
  • IL-22 Binding Protein Promotes the Disease Process in Multiple Sclerosis Hannes Lindahl, André O
    IL-22 Binding Protein Promotes the Disease Process in Multiple Sclerosis Hannes Lindahl, André O. Guerreiro-Cacais, Sahl Khalid Bedri, Mathias Linnerbauer, Magdalena Lindén, Nada This information is current as Abdelmagid, Karolina Tandre, Claire Hollins, Lorraine of September 24, 2021. Irving, Colin Glover, Clare Jones, Lars Alfredsson, Lars Rönnblom, Ingrid Kockum, Mohsen Khademi, Maja Jagodic and Tomas Olsson J Immunol published online 10 July 2019 Downloaded from http://www.jimmunol.org/content/early/2019/07/09/jimmun ol.1900400 Supplementary http://www.jimmunol.org/content/suppl/2019/07/10/jimmunol.190040 http://www.jimmunol.org/ Material 0.DCSupplemental 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 September 24, 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 © 2019 by The American Association of Immunologists, Inc. All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. Published
    [Show full text]
  • The Interleukin 22 Pathway Interacts with Mutant KRAS to Promote Poor Prognosis in Colon Cancer
    Author Manuscript Published OnlineFirst on May 19, 2020; DOI: 10.1158/1078-0432.CCR-19-1086 Author manuscripts have been peer reviewed and accepted for publication but have not yet been edited. The interleukin 22 pathway interacts with mutant KRAS to promote poor prognosis in colon cancer Authors: Sarah McCuaig1, David Barras,2, Elizabeth Mann1, Matthias Friedrich1, Samuel Bullers1, Alina Janney1, Lucy C. Garner1, Enric Domingo3, Viktor Hendrik Koelzer3,4,5, Mauro Delorenzi2,6,7, Sabine Tejpar8, Timothy Maughan9, Nathaniel R. West1, Fiona Powrie1 Affiliations: 1 Kennedy Institute of Rheumatology, University of Oxford, Oxford UK. 2 SIB Swiss Institute of Bioinformatics, Bioinformatics Core Facility, Lausanne, Switzerland. 3Department of Oncology, University of Oxford, Oxford UK. 4Nuffield Department of Medicine, University of Oxford, Oxford UK. 5Department of Pathology and Molecular Pathology, University and University Hospital Zurich, Zurich Switzerland. 6 Ludwig Center for Cancer Research, University of Lausanne, Lausanne, Switzerland. 7 Department of Oncology, Faculty of Biology and Medicine, University of Lausanne, Lausanne Switzerland. 8 Molecular Digestive Oncology, KU Leuven, Belgium. 9 CRUK/MRC Oxford Institute for Radiation Oncology, University of Oxford, Oxford, UK. Downloaded from clincancerres.aacrjournals.org on September 26, 2021. © 2020 American Association for Cancer Research. Author Manuscript Published OnlineFirst on May 19, 2020; DOI: 10.1158/1078-0432.CCR-19-1086 Author manuscripts have been peer reviewed and accepted for publication but have not yet been edited. Correspondence to: Professor Fiona Powrie; Kennedy Institute of Rheumatology, University of Oxford, Roosevelt Drive, Headington, Oxford, OX3 7YF, UK. Email: [email protected] Conflicts of Interest: S.M., N.R.W., and F.P.
    [Show full text]
  • Igs Cells Recognize Bacteria with Polyreactive Memory B +Iga
    Circulating Human CD27−IgA+ Memory B Cells Recognize Bacteria with Polyreactive Igs This information is current as Magdalena A. Berkowska, Jean-Nicolas Schickel, Christina of October 2, 2021. Grosserichter-Wagener, Dick de Ridder, Yen Shing Ng, Jacques J. M. van Dongen, Eric Meffre and Menno C. van Zelm J Immunol 2015; 195:1417-1426; Prepublished online 6 July 2015; doi: 10.4049/jimmunol.1402708 Downloaded from http://www.jimmunol.org/content/195/4/1417 Supplementary http://www.jimmunol.org/content/suppl/2015/07/03/jimmunol.140270 http://www.jimmunol.org/ Material 8.DCSupplemental References This article cites 57 articles, 31 of which you can access for free at: http://www.jimmunol.org/content/195/4/1417.full#ref-list-1 Why The JI? Submit online. by guest on October 2, 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 © 2015 by The American Association of Immunologists, Inc. All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. The Journal of Immunology Circulating Human CD272IgA+ Memory B Cells Recognize Bacteria with Polyreactive Igs Magdalena A.
    [Show full text]
  • 1714 Gene Comprehensive Cancer Panel Enriched for Clinically Actionable Genes with Additional Biologically Relevant Genes 400-500X Average Coverage on Tumor
    xO GENE PANEL 1714 gene comprehensive cancer panel enriched for clinically actionable genes with additional biologically relevant genes 400-500x average coverage on tumor Genes A-C Genes D-F Genes G-I Genes J-L AATK ATAD2B BTG1 CDH7 CREM DACH1 EPHA1 FES G6PC3 HGF IL18RAP JADE1 LMO1 ABCA1 ATF1 BTG2 CDK1 CRHR1 DACH2 EPHA2 FEV G6PD HIF1A IL1R1 JAK1 LMO2 ABCB1 ATM BTG3 CDK10 CRK DAXX EPHA3 FGF1 GAB1 HIF1AN IL1R2 JAK2 LMO7 ABCB11 ATR BTK CDK11A CRKL DBH EPHA4 FGF10 GAB2 HIST1H1E IL1RAP JAK3 LMTK2 ABCB4 ATRX BTRC CDK11B CRLF2 DCC EPHA5 FGF11 GABPA HIST1H3B IL20RA JARID2 LMTK3 ABCC1 AURKA BUB1 CDK12 CRTC1 DCUN1D1 EPHA6 FGF12 GALNT12 HIST1H4E IL20RB JAZF1 LPHN2 ABCC2 AURKB BUB1B CDK13 CRTC2 DCUN1D2 EPHA7 FGF13 GATA1 HLA-A IL21R JMJD1C LPHN3 ABCG1 AURKC BUB3 CDK14 CRTC3 DDB2 EPHA8 FGF14 GATA2 HLA-B IL22RA1 JMJD4 LPP ABCG2 AXIN1 C11orf30 CDK15 CSF1 DDIT3 EPHB1 FGF16 GATA3 HLF IL22RA2 JMJD6 LRP1B ABI1 AXIN2 CACNA1C CDK16 CSF1R DDR1 EPHB2 FGF17 GATA5 HLTF IL23R JMJD7 LRP5 ABL1 AXL CACNA1S CDK17 CSF2RA DDR2 EPHB3 FGF18 GATA6 HMGA1 IL2RA JMJD8 LRP6 ABL2 B2M CACNB2 CDK18 CSF2RB DDX3X EPHB4 FGF19 GDNF HMGA2 IL2RB JUN LRRK2 ACE BABAM1 CADM2 CDK19 CSF3R DDX5 EPHB6 FGF2 GFI1 HMGCR IL2RG JUNB LSM1 ACSL6 BACH1 CALR CDK2 CSK DDX6 EPOR FGF20 GFI1B HNF1A IL3 JUND LTK ACTA2 BACH2 CAMTA1 CDK20 CSNK1D DEK ERBB2 FGF21 GFRA4 HNF1B IL3RA JUP LYL1 ACTC1 BAG4 CAPRIN2 CDK3 CSNK1E DHFR ERBB3 FGF22 GGCX HNRNPA3 IL4R KAT2A LYN ACVR1 BAI3 CARD10 CDK4 CTCF DHH ERBB4 FGF23 GHR HOXA10 IL5RA KAT2B LZTR1 ACVR1B BAP1 CARD11 CDK5 CTCFL DIAPH1 ERCC1 FGF3 GID4 HOXA11 IL6R KAT5 ACVR2A
    [Show full text]
  • Wound-Healing Markers Revealed by Proximity Extension Assay in Tears of Patients Following Glaucoma Surgery
    International Journal of Molecular Sciences Article Wound-Healing Markers Revealed by Proximity Extension Assay in Tears of Patients following Glaucoma Surgery Éva Cs˝osz 1,2,* , Noémi Tóth 3, Eszter Deák 1,3, Adrienne Csutak 3,† and József T˝ozsér 1,2,† 1 Biomarker Research Group, Department of Biochemistry and Molecular Biology, Faculty of Medicine, University of Debrecen, Egyetem ter 1., 4032 Debrecen, Hungary; [email protected] (E.D.); [email protected] (J.T.) 2 Proteomics Core Facility, Department of Biochemistry and Molecular Biology, Faculty of Medicine, University of Debrecen, Egyetem ter 1., 4032 Debrecen, Hungary 3 Department of Ophthalmology, Faculty of Medicine, University of Debrecen, Nagyerdei krt. 98., 4032 Debrecen, Hungary; [email protected] (N.T.); [email protected] (A.C.) * Correspondence: [email protected]; Tel.: +36-52-416-432 † These authors contributed equally to this work. Received: 15 October 2018; Accepted: 11 December 2018; Published: 18 December 2018 Abstract: Tears are a constantly available and highly valuable body fluid collectable by non-invasive techniques. Although it can give information on ocular status and be used for follow-ups, tear analysis is challenging due to the low amount of sample that is available. Proximity extension assay (PEA) allows for a sensitive and scalable analysis of multiple proteins in a single run from a one-µL sample, so we applied this technique and examined the amount of 184 proteins in tears collected at different time points after trabeculectomy. The success rate of this surgical intervention highly depends on proper wound healing; therefore, information on the process is indispensable.
    [Show full text]
  • Development and Validation of a Protein-Based Risk Score for Cardiovascular Outcomes Among Patients with Stable Coronary Heart Disease
    Supplementary Online Content Ganz P, Heidecker B, Hveem K, et al. Development and validation of a protein-based risk score for cardiovascular outcomes among patients with stable coronary heart disease. JAMA. doi: 10.1001/jama.2016.5951 eTable 1. List of 1130 Proteins Measured by Somalogic’s Modified Aptamer-Based Proteomic Assay eTable 2. Coefficients for Weibull Recalibration Model Applied to 9-Protein Model eFigure 1. Median Protein Levels in Derivation and Validation Cohort eTable 3. Coefficients for the Recalibration Model Applied to Refit Framingham eFigure 2. Calibration Plots for the Refit Framingham Model eTable 4. List of 200 Proteins Associated With the Risk of MI, Stroke, Heart Failure, and Death eFigure 3. Hazard Ratios of Lasso Selected Proteins for Primary End Point of MI, Stroke, Heart Failure, and Death eFigure 4. 9-Protein Prognostic Model Hazard Ratios Adjusted for Framingham Variables eFigure 5. 9-Protein Risk Scores by Event Type This supplementary material has been provided by the authors to give readers additional information about their work. Downloaded From: https://jamanetwork.com/ on 10/02/2021 Supplemental Material Table of Contents 1 Study Design and Data Processing ......................................................................................................... 3 2 Table of 1130 Proteins Measured .......................................................................................................... 4 3 Variable Selection and Statistical Modeling ........................................................................................
    [Show full text]
  • Differentially Methylated Genes
    10/30/2013 Disclosures Key Rheumatoid Arthritis-Associated Pathogenic Pathways Revealed by Integrative Analysis of RA Omics Datasets Consultant: IGNYTA Funding: Rheumatology Research Foundation By John W. Whitaker, Wei Wang and Gary S. Firestein DNA methylation and gene regulation The RA methylation signature in FLS DNA methylation – DNMT1 (maintaining methylation) OA – DNMT3a, 3b (de novo methylation) RA % of CpG methylation: 0% 100% Nakano et al. 2013 ARD AA06 AANAT AARS ABCA6 ABCC12 ABCG1 ABHD8 ABL2 ABR ABRA ACACA ACAN ACAP3 ACCSL ACN9 ACOT7 ACOX2 ACP5 ACP6 ACPP ACSL1 ACSL3 ACSM5 ACVRL1 ADAM10 ADAM32 ADAM33 ADAMTS12 ADAMTS15 ADAMTS19 ADAMTS4 ADAT3 ADCK4 ADCK5 ADCY2 ADCY3 ADCY6 ADORA1 ADPGK ADPRHL1 ADTRP AFAP1 AFAP1L2 AFF3 AFG3L1P AGAP11 AGER AGTR1 AGXT AIF1L AIM2 AIRE AJUBA AK4 AKAP12 AKAP2 AKR1C2 AKR1E2 AKT2 ALAS1 ALDH1L1-AS1 ALDH3A1 ALDH3B1 ALDH8A1 ALDOB ALDOC ALOX12 ALPK3 ALS2CL ALX4 AMBRA1 AMPD2 AMPD3 ANGPT1 ANGPT2 ANGPTL5 ANGPTL6 ANK1 ANKMY2 ANKRD29 ANKRD37 ANKRD53 ANO3 ANO6 ANO7 ANP32C ANXA6 ANXA8L2 AP1G1 AP2A2 AP2M1 AP5B1 APBA2 APC APCDD1 APOBEC3B APOBEC3G APOC1 APOH APOL6 APOLD1 APOM AQP1 AQP10 AQP6 AQP9 ARAP1 ARHGAP24 ARHGAP42 ARHGEF19 ARHGEF25 ARHGEF3 ARHGEF37 ARHGEF7 ARL4C ARL6IP 5 ARL8B ARMC3 ARNTL2 ARPP21 ARRB1 ARSI ASAH2B ASB10 ASB2 ASCL2 ASIC4 ASPH ATF3 ATF7 ATL1 ATL3 ATP10A ATP1A1 ATP1A4 ATP2C1 ATP5A1 ATP5EP2 ATP5L2 ATP6V0CP3 ATP6V1C1 ATP6V1E2 ATXN7L1 ATXN7L2 AVPI1 AXIN2 B3GNT7 B3GNT8 B3GNTL1 BACH1 BAG3 Differential methylated genes in RA FLS BAIAP2L2 BANP BATF BATF2 BBS2 BCAS4 BCAT1 BCL7C BDKRB2 BEGAIN BEST1 BEST3
    [Show full text]
  • Supporting Information
    Supporting Information Voigt et al. 10.1073/pnas.1705165114 SI Materials and Methods the HTCR includes obtaining written informed consent from all Mice. BALB/c mice were purchased from Janvier. C57BL/6 mice patients with lung cancer and has been approved by the Ethics were purchased from Charles River. Mice were 5 wk old at the Committee of the Medical Faculty, LMU Munich (no. 025-12) and − − onset of experiments. Spleens from IL-1R / mice were provided by the Bavarian State Medical Association. All operations of from T. Stöger, Helmholtz Center Munich, Munich, and spleens Biobank are certified according to ISO 9001:2008 (57). Written − − from IL-23 / mice were a gift from K. Savvatis, Charité, Berlin. informed consent was obtained from all patients with breast cancer before collection of specimens, in line with the respective in- Cell Lines. The murine lung cancer cell line 1 (Line-1) was kindly stitutional policies and in accordance with to the Declaration of provided by Nejat K. Egilmez, University of Louisville, Louisville, Helsinki. Tumor specimens were obtained from patients un- KY (55), and cells were cultured in complete RPMI 1640 medium dergoing clinically indicated surgery. Histological analysis of (Lonza). If not stated otherwise, growth media used were supple- NSCLC or breast cancer was made by a pathologist as part of mented with 10% FBS, 100 μg/mL streptomycin, 1 IU/mL peni- standard of care. Ethical approval was obtained from the Ethics cillin, and 2 mM L-glutamine (Life Technologies). The 4T1murine Committee of the Medical Faculty, LMU Munich (reference breast cancer cell line was kindly provided by Maria Wartenberg, nos.
    [Show full text]
  • Human Colon Cancer Primer Library
    Human Colon Cancer Primer Library Catalog No: HCCR-1 Supplier: RealTimePrimers Lot No: XXXXX Supplied as: solid Stability: store at -20°C Description Contains 88 primer sets directed against cytokine and chemokine receptor genes and 8 housekeeping gene primer sets. Provided in a 96-well microplate (20 ul - 10 uM). Perform up to 100 PCR arrays (based on 20 ul assay volume per reaction). Just add cDNA template and SYBR green master mix. Gene List: • CCR1 chemokine (C-C motif) receptor 1 • IL11RA interleukin 11 receptor, alpha • CCR2 chemokine (C-C motif) receptor 2 • IL11RB interleukin 11 receptor, beta • CCR3 chemokine (C-C motif) receptor 3 • IL12RB1 interleukin 12 receptor, beta 1 • CCR4 chemokine (C-C motif) receptor 4 • IL12RB2 interleukin 12 receptor, beta 2 • CCR5 chemokine (C-C motif) receptor 5 • IL13RA1 interleukin 13 receptor, alpha 1 • CCR6 chemokine (C-C motif) receptor 6 • IL13RA2 interleukin 13 receptor, alpha 2 • CCR7 chemokine (C-C motif) receptor 7 • IL15RA interleukin 15 receptor, alpha • CCR8 chemokine (C-C motif) receptor 8 • IL15RB interleukin 15 receptor, beta • CCR9 chemokine (C-C motif) receptor 9 • IL17RA interleukin 17 receptor A • CCR10 chemokine (C-C motif) receptor 10 • IL17RB interleukin 17 receptor B • CX3CR1 chemokine (C-X3-C motif) receptor 1 • IL17RC interleukin 17 receptor C • CXCR1 chemokine (C-X-C motif) receptor 1 • IL17RD interleukin 17 receptor D • CXCR2 chemokine (C-X-C motif) receptor 2 • IL17RE interleukin 17 receptor E • CXCR3 chemokine (C-X-C motif) receptor 3 • IL18R1 interleukin 18 receptor
    [Show full text]
  • CX3CR1 Engagement by Respiratory Syncytial Virus Leads to Induction of Nucleolin And
    bioRxiv preprint doi: https://doi.org/10.1101/2020.07.29.227967; this version posted July 30, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-NC-ND 4.0 International license. 1 RESEARCH ARTICLE 2 3 CX3CR1 Engagement by Respiratory Syncytial Virus Leads to Induction of Nucleolin and 4 Dysregulation of Cilia-related Genes 5 6 Christopher S. Andersona*, Tatiana Chirkovab*, Christopher G. Slaunwhite, Xing Qiuc, Edward E. Walshd, 7 Larry J. Andersonb# and Thomas J. Mariania# 8 9 aDepartments of Pediatrics, University of Rochester Medical Center, Rochester, NY. 10 bEmory University Department of Pediatrics and Children’s Healthcare of Atlanta, Atlanta, GA. 11 cDepartment of Biostatistics and Computational Biology 12 dDepartment of Medicine, University of Rochester Medical Center, Rochester, NY. 13 *contributed equally to this work 14 #corresponding authors 15 16 Address for Correspondence: 17 Thomas J. Mariani, PhD 18 Professor of Pediatrics 19 Division of Neonatology and 20 Pediatric Molecular and Personalized Medicine Program 21 University of Rochester Medical Center 22 601 Elmwood Ave, Box 850 23 Rochester, NY 14642, USA. 24 Phone: 585-276-4616; Fax: 585-276-2643; 25 E-mail: [email protected] 26 1 bioRxiv preprint doi: https://doi.org/10.1101/2020.07.29.227967; this version posted July 30, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity.
    [Show full text]
  • IL-21) Receptor Is a Negative Feedback Regulator of IL-21 Signaling
    View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Elsevier - Publisher Connector FEBS Letters 585 (2011) 1835–1840 journal homepage: www.FEBSLetters.org Caspase-8 cleavage of the interleukin-21 (IL-21) receptor is a negative feedback regulator of IL-21 signaling Tatsuya Akagi a, Kouhei Shimizu a, Shoukichi Takahama b, Takahiro Iwasaki b, Kazuhiro Sakamaki c, ⇑ ⇑ Yaeta Endo a,b,d,e, , Tatsuya Sawasaki a,b,d,e, a Cell-Free Science and Technology Research Center, Ehime University, 3 Bunkyo-cho, Matsuyama, Ehime 790-8577, Japan b The Venture Business Laboratory, Ehime University, 3 Bunkyo-cho, Matsuyama, Ehime 790-8577, Japan c Department of Animal Development and Physiology, Graduate School of Biostudies, Kyoto University, Kyoto 606-8501, Japan d Proteo-Medicine Research Center, Ehime University, Toon, Ehime 791-0295, Japan e RIKEN Systems and Structural Biology Center, 1-7-22 Suehiro-cho, Tsurumi, Yokohama 230-0045, Japan article info abstract Article history: We screened a library of human single-transmembrane proteins (sTMPs), produced by a cell-free Received 1 February 2011 system, using a luminescent assay to identify those that can be cleaved by caspase-8 (CASP8). Of Revised 5 April 2011 the 407 sTMPs screened, only the interleukin-21 receptor (IL21R), vezatin (VEZT), and carbonic Accepted 13 April 2011 anhydrase XIV were cleaved at Asp344, Asp655 and Asp53, respectively. We confirmed that IL21R Available online 20 April 2011 and VEZT were also cleaved in apoptotic HeLa cells with the cleavage sites. Interestingly, IL21R Edited by Vladimir Skulachev was cleaved within 30 min after apoptosis induction.
    [Show full text]
  • Engineered Type 1 Regulatory T Cells Designed for Clinical Use Kill Primary
    ARTICLE Acute Myeloid Leukemia Engineered type 1 regulatory T cells designed Ferrata Storti Foundation for clinical use kill primary pediatric acute myeloid leukemia cells Brandon Cieniewicz,1* Molly Javier Uyeda,1,2* Ping (Pauline) Chen,1 Ece Canan Sayitoglu,1 Jeffrey Mao-Hwa Liu,1 Grazia Andolfi,3 Katharine Greenthal,1 Alice Bertaina,1,4 Silvia Gregori,3 Rosa Bacchetta,1,4 Norman James Lacayo,1 Alma-Martina Cepika1,4# and Maria Grazia Roncarolo1,2,4# Haematologica 2021 Volume 106(10):2588-2597 1Department of Pediatrics, Division of Stem Cell Transplantation and Regenerative Medicine, Stanford School of Medicine, Stanford, CA, USA; 2Stanford Institute for Stem Cell Biology and Regenerative Medicine, Stanford School of Medicine, Stanford, CA, USA; 3San Raffaele Telethon Institute for Gene Therapy, Milan, Italy and 4Center for Definitive and Curative Medicine, Stanford School of Medicine, Stanford, CA, USA *BC and MJU contributed equally as co-first authors #AMC and MGR contributed equally as co-senior authors ABSTRACT ype 1 regulatory (Tr1) T cells induced by enforced expression of interleukin-10 (LV-10) are being developed as a novel treatment for Tchemotherapy-resistant myeloid leukemias. In vivo, LV-10 cells do not cause graft-versus-host disease while mediating graft-versus-leukemia effect against adult acute myeloid leukemia (AML). Since pediatric AML (pAML) and adult AML are different on a genetic and epigenetic level, we investigate herein whether LV-10 cells also efficiently kill pAML cells. We show that the majority of primary pAML are killed by LV-10 cells, with different levels of sensitivity to killing. Transcriptionally, pAML sensitive to LV-10 killing expressed a myeloid maturation signature.
    [Show full text]