TSPAN4 Rabbit Pab

Total Page：16

File Type：pdf, Size：1020Kb

Leader in Biomolecular Solutions for Life Science TSPAN4 Rabbit pAb Catalog No.: A10253 Basic Information Background Catalog No. The protein encoded by this gene is a member of the transmembrane 4 superfamily, A10253 also known as the tetraspanin family. Most of these members are cell-surface proteins that are characterized by the presence of four hydrophobic domains. The proteins Observed MW mediate signal transduction events that play a role in the regulation of cell 26kDa development, activation, growth and motility. This encoded protein is a cell surface glycoprotein and is similar in sequence to its family member CD53 antigen. It is known to Calculated MW complex with integrins and other transmembrane 4 superfamily proteins. Alternatively 26kDa spliced transcript variants encoding different isoforms have been identified. Category Primary antibody Applications WB Cross-Reactivity Mouse, Rat Recommended Dilutions Immunogen Information WB 1:1000 - 1:2000 Gene ID Swiss Prot 7106 O14817 Immunogen Recombinant fusion protein containing a sequence corresponding to amino acids 107-201 of human TSPAN4 (NP_003262.1). Synonyms TSPAN4;NAG-2;NAG2;TETRASPAN;TM4SF7;TSPAN-4 Contact Product Information www.abclonal.com Source Isotype Purification Rabbit IgG Affinity purification Storage Store at -20℃. Avoid freeze / thaw cycles. Buffer: PBS with 0.02% sodium azide,50% glycerol,pH7.3. Validation Data Western blot analysis of extracts of various cell lines, using TSPAN4 antibody (A10253) at 1:1000 dilution. Secondary antibody: HRP Goat Anti-Rabbit IgG (H+L) (AS014) at 1:10000 dilution. Lysates/proteins: 25ug per lane. Blocking buffer: 3% nonfat dry milk in TBST. Detection: ECL Basic Kit (RM00020). Exposure time: 15s. Antibody | Protein | ELISA Kits | Enzyme | NGS | Service For research use only. Not for therapeutic or diagnostic purposes. Please visit http://abclonal.com for a complete listing of recommended products..

Copy Link

Recommended publications

Migrasome Formation Is Mediated by Assembly of Micron-Scale Tetraspanin Macrodomains
ARTICLES https://doi.org/10.1038/s41556-019-0367-5 Corrected: Publisher Correction Migrasome formation is mediated by assembly of micron-scale tetraspanin macrodomains Yuwei Huang1,2,6, Ben Zucker3,6, Shaojin Zhang1,2,6, Sharon Elias3, Yun Zhu4, Hui Chen5, Tianlun Ding1,2, Ying Li1,2, Yujie Sun4, Jizhong Lou5, Michael M. Kozlov 3* and Li Yu 1,2* Migrasomes are recently discovered cellular organelles that form as large vesicle-like structures on retraction fibres of migrat- ing cells. While the process of migrasome formation has been described before, the molecular mechanism underlying migra- some biogenesis remains unclear. Here, we propose that the mechanism of migrasome formation consists of the assembly of tetraspanin- and cholesterol-enriched membrane microdomains into micron-scale macrodomains, which swell into migra- somes. The major finding underlying the mechanism is that tetraspanins and cholesterol are necessary and sufficient for migra- some formation. We demonstrate the necessity of tetraspanins and cholesterol via live-cell experiments, and their sufficiency by generating migrasome-like structures in reconstituted membrane systems. We substantiate the mechanism by a theoretical model proposing that the key factor driving migrasome formation is the elevated membrane stiffness of the tetraspanin- and cholesterol-enriched macrodomains. Finally, the theoretical model was quantitatively validated by experimental demonstration of the membrane-stiffening effect of tetraspanin 4 and cholesterol. igrasomes are recently discovered cellular organelles whose To study whether the TSPAN4 expression level can affect mig- formation is closely associated with cell migration. When rasome formation, we established three normal rat kidney (NRK) Mcells crawl on extracellular substrates, long membrane pro- epithelial cell lines that stably express different levels of TSPAN4 jections, referred to as retraction fibres (RFs), are pulled out of the and green fluorescent protein (GFP) (Fig.
[Show full text]
Human Induced Pluripotent Stem Cell–Derived Podocytes Mature Into Vascularized Glomeruli Upon Experimental Transplantation
BASIC RESEARCH www.jasn.org Human Induced Pluripotent Stem Cell–Derived Podocytes Mature into Vascularized Glomeruli upon Experimental Transplantation † Sazia Sharmin,* Atsuhiro Taguchi,* Yusuke Kaku,* Yasuhiro Yoshimura,* Tomoko Ohmori,* ‡ † ‡ Tetsushi Sakuma, Masashi Mukoyama, Takashi Yamamoto, Hidetake Kurihara,§ and | Ryuichi Nishinakamura* *Department of Kidney Development, Institute of Molecular Embryology and Genetics, and †Department of Nephrology, Faculty of Life Sciences, Kumamoto University, Kumamoto, Japan; ‡Department of Mathematical and Life Sciences, Graduate School of Science, Hiroshima University, Hiroshima, Japan; §Division of Anatomy, Juntendo University School of Medicine, Tokyo, Japan; and |Japan Science and Technology Agency, CREST, Kumamoto, Japan ABSTRACT Glomerular podocytes express proteins, such as nephrin, that constitute the slit diaphragm, thereby contributing to the ﬁltration process in the kidney. Glomerular development has been analyzed mainly in mice, whereas analysis of human kidney development has been minimal because of limited access to embryonic kidneys. We previously reported the induction of three-dimensional primordial glomeruli from human induced pluripotent stem (iPS) cells. Here, using transcription activator–like effector nuclease-mediated homologous recombination, we generated human iPS cell lines that express green ﬂuorescent protein (GFP) in the NPHS1 locus, which encodes nephrin, and we show that GFP expression facilitated accurate visualization of nephrin-positive podocyte formation in
[Show full text]
Genetic Defects in B-Cell Development and Their Clinical Consequences H Abolhassani,1,2 N Parvaneh,1 N Rezaei,1 L Hammarström,2 a Aghamohammadi1
REVIEWS Genetic Defects in B-Cell Development and Their Clinical Consequences H Abolhassani,1,2 N Parvaneh,1 N Rezaei,1 L Hammarström,2 A Aghamohammadi1 1Research Center for Immunodeficiencies, Pediatrics Center of Excellence, Children’s Medical Center, Tehran University of Medical Sciences, Tehran, Iran 2Division of Clinical Immunology, Department of Laboratory Medicine, Karolinska Institutet at Karolinska University Hospital Huddinge, Stockholm, Sweden n Abstract Expression of selected genes in hematopoietic stem cells has been identified as a regulator of differentiation of B cells in the liver and bone marrow. Moreover, naïve B cells expressing surface immunoglobulin need other types of genes for antigen-dependent development in secondary lymphoid organs. Many advanced molecular mechanisms underlying primary antibody deficiencies in humans have been described. We provide an overview of the mutations in genes known to be involved in B-cell development and their clinical consequences. Key words: Genetic disorder. B-cell development. Primary antibody deficiencies. Clinical phenotypes. n Resumen Se ha identificado la expresión de genes seleccionados en las células pluripotenciales de médula ósea como reguladores de la diferenciación de las células B en el hígado y en médula ósea. Sin embargo, las células B naïve que expresan inmunoglubulinas de superficie, necesitan otros tipos de genes para su desarrollo en los órganos linfoides secundarios dependienteS de antígeno. Se han descrito muchos mecanismos moleculares avanzados que subrayan las inmunodeficiencias en humanos y esta revisión constituye una visión general de la mutación en todos los genes conocidos involucrados en el desarrollo de las células B y sus consecuencias clínicas. Palabras clave: Alteraciones genéticas. Desarrollo de las células B.
[Show full text]
©Ferrata Storti Foundation
Original Articles T-cell/histiocyte-rich large B-cell lymphoma shows transcriptional features suggestive of a tolerogenic host immune response Peter Van Loo,1,2,3 Thomas Tousseyn,4 Vera Vanhentenrijk,4 Daan Dierickx,5 Agnieszka Malecka,6 Isabelle Vanden Bempt,4 Gregor Verhoef,5 Jan Delabie,6 Peter Marynen,1,2 Patrick Matthys,7 and Chris De Wolf-Peeters4 1Department of Molecular and Developmental Genetics, VIB, Leuven, Belgium; 2Department of Human Genetics, K.U.Leuven, Leuven, Belgium; 3Bioinformatics Group, Department of Electrical Engineering, K.U.Leuven, Leuven, Belgium; 4Department of Pathology, University Hospitals K.U.Leuven, Leuven, Belgium; 5Department of Hematology, University Hospitals K.U.Leuven, Leuven, Belgium; 6Department of Pathology, The Norwegian Radium Hospital, University of Oslo, Oslo, Norway, and 7Department of Microbiology and Immunology, Rega Institute for Medical Research, K.U.Leuven, Leuven, Belgium Citation: Van Loo P, Tousseyn T, Vanhentenrijk V, Dierickx D, Malecka A, Vanden Bempt I, Verhoef G, Delabie J, Marynen P, Matthys P, and De Wolf-Peeters C. T-cell/histiocyte-rich large B-cell lymphoma shows transcriptional features suggestive of a tolero- genic host immune response. Haematologica. 2010;95:440-448. doi:10.3324/haematol.2009.009647 The Online Supplementary Tables S1-5 are in separate PDF files Supplementary Design and Methods One microgram of total RNA was reverse transcribed using random primers and SuperScript II (Invitrogen, Merelbeke, Validation of microarray results by real-time quantitative Belgium), as recommended by the manufacturer. Relative reverse transcriptase polymerase chain reaction quantification was subsequently performed using the compar- Ten genes measured by microarray gene expression profil- ative CT method (see User Bulletin #2: Relative Quantitation ing were validated by real-time quantitative reverse transcrip- of Gene Expression, Applied Biosystems).
[Show full text]
Tetraspanins in the Regulation of Mast Cell Function
Medical Microbiology and Immunology (2020) 209:531–543 https://doi.org/10.1007/s00430-020-00679-x REVIEW Tetraspanins in the regulation of mast cell function Zane Orinska1 · Philipp M. Hagemann1 · Ivana Halova2 · Petr Draber2 Received: 17 February 2020 / Accepted: 6 May 2020 / Published online: 7 June 2020 © The Author(s) 2020 Abstract Mast cells (MCs) are long-living immune cells highly specialized in the storage and release of diferent biologically active compounds and are involved in the regulation of innate and adaptive immunity. MC degranulation and replacement of MC granules are accompanied by active membrane remodelling. Tetraspanins represent an evolutionary conserved family of transmembrane proteins. By interacting with lipids and other membrane and intracellular proteins, they are involved in organisation of membrane protein complexes and act as “molecular facilitators” connecting extracellular and cytoplasmic signaling elements. MCs express diferent tetraspanins and MC degranulation is accompanied by changes in membrane organisation. Therefore, tetraspanins are very likely involved in the regulation of MC exocytosis and membrane reorganisa- tion after degranulation. Antiviral response and production of exosomes are further aspects of MC function characterized by dynamic changes of membrane organization. In this review, we pay a particular attention to tetraspanin gene expression in diferent human and murine MC populations, discuss tetraspanin involvement in regulation of key MC signaling com- plexes, and analyze the potential contribution of tetraspanins to MC antiviral response and exosome production. In-depth knowledge of tetraspanin-mediated molecular mechanisms involved in diferent aspects of the regulation of MC response will be benefcial for patients with allergies, characterized by overwhelming MC reactions.
[Show full text]
1 SUPPLEMENTAL DATA Figure S1. Poly I:C Induces IFN-Β Expression
SUPPLEMENTAL DATA Figure S1. Poly I:C induces IFN-β expression and signaling. Fibroblasts were incubated in media with or without Poly I:C for 24 h. RNA was isolated and processed for microarray analysis. Genes showing >2-fold up- or down-regulation compared to control fibroblasts were analyzed using Ingenuity Pathway Analysis Software (Red color, up-regulation; Green color, down-regulation). The transcripts with known gene identifiers (HUGO gene symbols) were entered into the Ingenuity Pathways Knowledge Base IPA 4.0. Each gene identifier mapped in the Ingenuity Pathways Knowledge Base was termed as a focus gene, which was overlaid into a global molecular network established from the information in the Ingenuity Pathways Knowledge Base. Each network contained a maximum of 35 focus genes. 1 Figure S2. The overlap of genes regulated by Poly I:C and by IFN. Bioinformatics analysis was conducted to generate a list of 2003 genes showing >2 fold up or down- regulation in fibroblasts treated with Poly I:C for 24 h. The overlap of this gene set with the 117 skin gene IFN Core Signature comprised of datasets of skin cells stimulated by IFN (Wong et al, 2012) was generated using Microsoft Excel. 2 Symbol Description polyIC 24h IFN 24h CXCL10 chemokine (C-X-C motif) ligand 10 129 7.14 CCL5 chemokine (C-C motif) ligand 5 118 1.12 CCL5 chemokine (C-C motif) ligand 5 115 1.01 OASL 2'-5'-oligoadenylate synthetase-like 83.3 9.52 CCL8 chemokine (C-C motif) ligand 8 78.5 3.25 IDO1 indoleamine 2,3-dioxygenase 1 76.3 3.5 IFI27 interferon, alpha-inducible
[Show full text]
Table 4. 391 Probe Sets Still Rhythmic After Sleep Deprivation
Table 4. 391 probe sets still rhythmic after sleep deprivation Affymetrix ID Gene Symbol Description Accession time_sin time_cos adj.P.Val 1438211_s_at Dbp D site albumin promoter binding protein BB550183 -0.013 -0.877 1.44E-13 1418174_at Dbp D site albumin promoter binding protein BC018323 -0.036 -0.880 1.74E-13 1425099_a_at Arntl aryl hydrocarbon receptor nuclear translocator-like BC011080 0.135 0.418 1.02E-11 1416958_at Nr1d2 nuclear receptor subfamily 1, group D, member 2 NM_011584 -0.035 -0.397 7.53E-11 1421087_at Per3 period homolog 3 (Drosophila) NM_011067 -0.119 -0.477 3.46E-10 1450779_at Fabp7 fatty acid binding protein 7, brain NM_021272 0.433 0.404 3.82E-10 1424175_at Tef thyrotroph embryonic factor BC017689 -0.113 -0.279 1.39E-09 1435188_at Gm129 gene model 129, (NCBI) BB407125 -0.097 -0.667 4.17E-09 1417602_at Per2 period homolog 2 (Drosophila) AF035830 -0.460 -0.408 5.97E-09 1425560_a_at S100a16 S100 calcium binding protein A16 BC020031 0.228 0.194 5.97E-09 1435459_at Fmo2 flavin containing monooxygenase 2 BM936480 -0.255 -0.426 6.23E-09 1457350_at Per2 period homolog 2 (Drosophila) BG298986 -0.312 -0.485 7.81E-09 1445892_at Per2 Period homolog 2 (Drosophila) BM238318 -0.300 -0.432 1.50E-08 1448383_at Mmp14 matrix metallopeptidase 14 (membrane-inserted) NM_008608 0.082 0.474 3.74E-08 1456046_at Cd93 CD93 antigen AV319144 0.357 0.320 4.89E-08 1429286_at 1190003M12Rik RIKEN cDNA 1190003M12 gene AK004474 -0.511 -0.245 5.08E-08 similar to Putative RNA-binding protein 3 (RNA- 1422660_at LOC671237 AY052560 -0.269 -0.318 5.40E-08
[Show full text]
SF3B1-Mutated Chronic Lymphocytic Leukemia Shows Evidence Of
SF3B1-mutated chronic lymphocytic leukemia shows evidence of NOTCH1 pathway activation including CD20 downregulation by Federico Pozzo, Tamara Bittolo, Erika Tissino, Filippo Vit, Elena Vendramini, Luca Laurenti, Giovanni D'Arena, Jacopo Olivieri, Gabriele Pozzato, Francesco Zaja, Annalisa Chiarenza, Francesco Di Raimondo, Antonella Zucchetto, Riccardo Bomben, Francesca Maria Rossi, Giovanni Del Poeta, Michele Dal Bo, and Valter Gattei Haematologica 2020 [Epub ahead of print] Citation: Federico Pozzo, Tamara Bittolo, Erika Tissino, Filippo Vit, Elena Vendramini, Luca Laurenti, Giovanni D'Arena, Jacopo Olivieri, Gabriele Pozzato, Francesco Zaja, Annalisa Chiarenza, Francesco Di Raimondo, Antonella Zucchetto, Riccardo Bomben, Francesca Maria Rossi, Giovanni Del Poeta, Michele Dal Bo, and Valter Gattei SF3B1-mutated chronic lymphocytic leukemia shows evidence of NOTCH1 pathway activation including CD20 downregulation. Haematologica. 2020; 105:xxx doi:10.3324/haematol.2020.261891 Publisher's Disclaimer. E-publishing ahead of print is increasingly important for the rapid dissemination of science. Haematologica is, therefore, E-publishing PDF files of an early version of manuscripts that have completed a regular peer review and have been accepted for publication. E-publishing of this PDF file has been approved by the authors. After having E-published Ahead of Print, manuscripts will then undergo technical and English editing, typesetting, proof correction and be presented for the authors' final approval; the final version of the manuscript will
[Show full text]
Tubular P53 Regulates Multiple Genes to Mediate AKI
BASIC RESEARCH www.jasn.org Tubular p53 Regulates Multiple Genes to Mediate AKI † † † † † Dongshan Zhang,* Yu Liu,* Qingqing Wei, Yuqing Huo, Kebin Liu, Fuyou Liu,* and † Zheng Dong* *Departments of Emergency Medicine and Nephrology, Second Xiangya Hospital, Central South University, Changsha, Hunan, China; and †Department of Cellular Biology and Anatomy, Vascular Biology Center and Department of Biochemistry and Molecular Biology, Georgia Regents University and Charlie Norwood Veterans Affairs Medical Center, Augusta, Georgia ABSTRACT A pathogenic role of p53 in AKI was suggested a decade ago but remains controversial. Indeed, recent work indicates that inhibition of p53 protects against ischemic AKI in rats but exacerbates AKI in mice. One intriguing possibility is that p53 has cell type-specific roles in AKI. To determine the role of tubular p53, we generated two conditional gene knockout mouse models, in which p53 is specifically ablated from proximal tubules or other tubular segments, including distal tubules, loops of Henle, and medullary collecting ducts. Proximal tubule p53 knockout (PT-p53-KO) mice were resistant to ischemic and cisplatin nephrotoxic AKI, which was indicated by the analysis of renal function, histology, apoptosis, and inflammation. However, other tubular p53 knockout (OT-p53-KO) mice were sensitive to AKI. Mechanis- tically, AKI associated with the upregulation of several known p53 target genes, including Bax, p53- upregulated modulator of apoptosis-a, p21, and Siva, and this association was attenuated in PT-p53-KO mice. In global expression analysis, ischemic AKI induced 371 genes in wild-type kidney cortical tissues, but the induction of 31 of these genes was abrogated in PT-p53-KO tissues.
[Show full text]
Supplementary Table 1 Double Treatment Vs Single Treatment
Supplementary table 1 Double treatment vs single treatment Probe ID Symbol Gene name P value Fold change TC0500007292.hg.1 NIM1K NIM1 serine/threonine protein kinase 1.05E-04 5.02 HTA2-neg-47424007_st NA NA 3.44E-03 4.11 HTA2-pos-3475282_st NA NA 3.30E-03 3.24 TC0X00007013.hg.1 MPC1L mitochondrial pyruvate carrier 1-like 5.22E-03 3.21 TC0200010447.hg.1 CASP8 caspase 8, apoptosis-related cysteine peptidase 3.54E-03 2.46 TC0400008390.hg.1 LRIT3 leucine-rich repeat, immunoglobulin-like and transmembrane domains 3 1.86E-03 2.41 TC1700011905.hg.1 DNAH17 dynein, axonemal, heavy chain 17 1.81E-04 2.40 TC0600012064.hg.1 GCM1 glial cells missing homolog 1 (Drosophila) 2.81E-03 2.39 TC0100015789.hg.1 POGZ Transcript Identified by AceView, Entrez Gene ID(s) 23126 3.64E-04 2.38 TC1300010039.hg.1 NEK5 NIMA-related kinase 5 3.39E-03 2.36 TC0900008222.hg.1 STX17 syntaxin 17 1.08E-03 2.29 TC1700012355.hg.1 KRBA2 KRAB-A domain containing 2 5.98E-03 2.28 HTA2-neg-47424044_st NA NA 5.94E-03 2.24 HTA2-neg-47424360_st NA NA 2.12E-03 2.22 TC0800010802.hg.1 C8orf89 chromosome 8 open reading frame 89 6.51E-04 2.20 TC1500010745.hg.1 POLR2M polymerase (RNA) II (DNA directed) polypeptide M 5.19E-03 2.20 TC1500007409.hg.1 GCNT3 glucosaminyl (N-acetyl) transferase 3, mucin type 6.48E-03 2.17 TC2200007132.hg.1 RFPL3 ret finger protein-like 3 5.91E-05 2.17 HTA2-neg-47424024_st NA NA 2.45E-03 2.16 TC0200010474.hg.1 KIAA2012 KIAA2012 5.20E-03 2.16 TC1100007216.hg.1 PRRG4 proline rich Gla (G-carboxyglutamic acid) 4 (transmembrane) 7.43E-03 2.15 TC0400012977.hg.1 SH3D19
[Show full text]
Tetraspanin CD9 Participates in Dysmegakaryopoiesis and Stromal Interactions in Primary Myelofibrosis
Myeloproliferative Disorders SUPPLEMENTARY APPENDIX Tetraspanin CD9 participates in dysmegakaryopoiesis and stromal interactions in primary myelofibrosis Christophe Desterke, 1,2 Christophe Martinaud, 1,3 Bernadette Guerton, 1 Lisa Pieri, 4 Costanza Bogani, 4 Denis Clay, 1,2 Fred - eric Torossian, 1,2 Jean-Jacques Lataillade, 1,4 Hans C. Hasselbach, 5 Heinz Gisslinger, 6 Jean-Loup Demory, 7,8 Brigitte Du - priez, 8,9 Claude Boucheix, 2,10 Eric Rubinstein, 2,10 Sophie Amsellem, 11 Alessandro M. Vannucchi, 4 and Marie-Caroline Le Bousse-Kerdilès 1,2,8 1INSERM UMR-S1197, Paul Brousse Hospital, Paris-Sud University, Villejuif, France; 2INSERM UMS33, Paul Brousse Hospital, Paris- Sud University, Villejuif, France; 3CTS of Army, Percy Hospital, Clamart, France; 4Department of Experimental and Clinical Medicine, University of Florence, Italy; 5Department of Hematology, Herlev University Hospital, Copenhagen, Denmark; 6Department of Hema - tology, University Klinik Fur Innere Medizin, Vienna, Austria; 7Université Catholique de Lille, France; 8French Intergroup on Myeloprolif - erative Neoplasms (FIM), France; 9Department of Hematology, Dr Schaffner Hospital, Lens, France; 10 Inserm U935, Paul Brousse Hospital, Paris-Sud University, Villejuif, France; and 11 Department of Hematology, Gustave Roussy Institute, Villejuif, France ©2015 Ferrata Storti Foundation. This is an open-access paper. doi:10.3324/haematol.2014.118497 Manuscript received on October 2, 2014. Manuscript accepted on March 23, 2015. Correspondence: [email protected]
[Show full text]
Autocrine IFN Signaling Inducing Profibrotic Fibroblast Responses By
Downloaded from http://www.jimmunol.org/ by guest on September 23, 2021 Inducing is online at: average * The Journal of Immunology , 11 of which you can access for free at: 2013; 191:2956-2966; Prepublished online 16 from submission to initial decision 4 weeks from acceptance to publication August 2013; doi: 10.4049/jimmunol.1300376 http://www.jimmunol.org/content/191/6/2956 A Synthetic TLR3 Ligand Mitigates Profibrotic Fibroblast Responses by Autocrine IFN Signaling Feng Fang, Kohtaro Ooka, Xiaoyong Sun, Ruchi Shah, Swati Bhattacharyya, Jun Wei and John Varga J Immunol cites 49 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/2013/08/20/jimmunol.130037 6.DC1 This article http://www.jimmunol.org/content/191/6/2956.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 © 2013 by The American Association of Immunologists, Inc. All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. This information is current as of September 23, 2021. The Journal of Immunology A Synthetic TLR3 Ligand Mitigates Proﬁbrotic Fibroblast Responses by Inducing Autocrine IFN Signaling Feng Fang,* Kohtaro Ooka,* Xiaoyong Sun,† Ruchi Shah,* Swati Bhattacharyya,* Jun Wei,* and John Varga* Activation of TLR3 by exogenous microbial ligands or endogenous injury-associated ligands leads to production of type I IFN.
[Show full text]