Expression of Interferon Regulatory Factor 5 Is Regulated by the Sp1 Transcription Factor
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Stat4 Consensus and Mutant Oligonucleotides
SANTA CRUZ BIOTECHNOLOGY, INC. Stat4 Consensus and Mutant Oligonucleotides BACKGROUND PRODUCT Electrophoretic mobility shift assays (EMSAs), also known as gel shift assays, Stat4 CONSENSUS OLIGONUCLEOTIDE: sc-2569 provide a relatively straightforward and sensitive method for studying bind- ■ binding site for Stat4 (3) ing interactions between transcription factors and consensus DNA binding elements. For such studies, DNA probes are provided as double-stranded 5’ — GAG CCT GA T TTC CCC GAA AT G ATG AGC TAG — 3’ oligonucleotides designed with 5' OH blunt ends to facilitate labeling to high 3’ — CTC GGA C T A AAG GGG CTT TA C TAC TCG ATC — 5’ specific activity with polynucleotide kinase. These are constructed both with Stat4 MUTANT OLIGONUCLEOTIDE: sc-2570 specific DNA binding consensus sequences for various transcription factors ■ identical to sc-2569 with the exception of a “CCC” “TTT” substitution in and as control or “mutant” probes in which one or more nucleotides mapping → the Stat4 binding motif (3) within the consensus binding site has been substituted. 5’ — GAG CCT GA T TTC TTT GAA AT G ATG AGC TAG — 3’ REFERENCES 3’ — CTC GGA C T A AAG AAA CTT TA C TAC TCG ATC — 5’ 1. Dignam, J.D., et al. 1983. Accurate transcription initiation by RNA poly- merase II in a soluble extract from isolated mammalian nuclei. Nucleic SELECT PRODUCT CITATIONS Acids Res. 11: 1475-1489. 1. Ahn, H.J., et al. 1998. Requirement for distinct Janus kinases and STAT 2. Murre, C., et al. 1991. B cell- and myocyte-specific E2-box-binding factors proteins in T cell proliferation versus IFN-g production following IL-12 contain E12/E47-like subunits. -
Comprehensive Study of Nuclear Receptor DNA Binding Provides a Revised Framework for Understanding Receptor Specificity
ARTICLE https://doi.org/10.1038/s41467-019-10264-3 OPEN Comprehensive study of nuclear receptor DNA binding provides a revised framework for understanding receptor specificity Ashley Penvose 1,2,4, Jessica L. Keenan 2,3,4, David Bray2,3, Vijendra Ramlall 1,2 & Trevor Siggers 1,2,3 The type II nuclear receptors (NRs) function as heterodimeric transcription factors with the retinoid X receptor (RXR) to regulate diverse biological processes in response to endogenous 1234567890():,; ligands and therapeutic drugs. DNA-binding specificity has been proposed as a primary mechanism for NR gene regulatory specificity. Here we use protein-binding microarrays (PBMs) to comprehensively analyze the DNA binding of 12 NR:RXRα dimers. We find more promiscuous NR-DNA binding than has been reported, challenging the view that NR binding specificity is defined by half-site spacing. We show that NRs bind DNA using two distinct modes, explaining widespread NR binding to half-sites in vivo. Finally, we show that the current models of NR specificity better reflect binding-site activity rather than binding-site affinity. Our rich dataset and revised NR binding models provide a framework for under- standing NR regulatory specificity and will facilitate more accurate analyses of genomic datasets. 1 Department of Biology, Boston University, Boston, MA 02215, USA. 2 Biological Design Center, Boston University, Boston, MA 02215, USA. 3 Bioinformatics Program, Boston University, Boston, MA 02215, USA. 4These authors contributed equally: Ashley Penvose, Jessica L. Keenan. Correspondence -
IRF5 Gene Interferon Regulatory Factor 5
IRF5 gene interferon regulatory factor 5 Normal Function The protein produced from the IRF5 gene, called interferon regulatory factor 5 (IRF5), acts as a transcription factor, which means that it attaches (binds) to specific regions of DNA and helps control the activity of certain genes. When a virus is recognized in the cell, the IRF5 gene is turned on (activated), which leads to the production of IRF5 protein. The protein binds to specific regions of DNA that regulate the activity of genes that produce interferons and other cytokines. Cytokines are proteins that help fight infection by promoting inflammation and regulating the activity of immune system cells. In particular, interferons control the activity of genes that help block the replication of viruses, and they stimulate the activity of certain immune system cells known as natural killer cells. Health Conditions Related to Genetic Changes Systemic scleroderma Several normal variations in the IRF5 gene have been associated with an increased risk of developing systemic scleroderma, which is an autoimmune disorder characterized by the buildup of scar tissue (fibrosis) in the skin and internal organs. Although the IRF5 gene is known to stimulate the immune system in response to viruses, it is unknown how the gene variations contribute to the increased risk of systemic scleroderma. Researchers believe that a combination of genetic and environmental factors may play a role in development of the condition. Rheumatoid arthritis MedlinePlus Genetics provides information about Rheumatoid arthritis Systemic lupus erythematosus MedlinePlus Genetics provides information about Systemic lupus erythematosus Ulcerative colitis MedlinePlus Genetics provides information about Ulcerative colitis Reprinted from MedlinePlus Genetics (https://medlineplus.gov/genetics/) 1 Autoimmune disorders Studies have associated normal variations in the IRF5 gene with an increased risk of several autoimmune disorders. -
Entinostat Augments NK Cell Functions Via Epigenetic Upregulation of IFIT1-STING-STAT4 Pathway
www.oncotarget.com Oncotarget, 2020, Vol. 11, (No. 20), pp: 1799-1815 Research Paper Entinostat augments NK cell functions via epigenetic upregulation of IFIT1-STING-STAT4 pathway John M. Idso1, Shunhua Lao1, Nathan J. Schloemer1,2, Jeffrey Knipstein2, Robert Burns3, Monica S. Thakar1,2,* and Subramaniam Malarkannan1,2,4,5,* 1Laboratory of Molecular Immunology and Immunotherapy, Blood Research Institute, Versiti, Milwaukee, WI, USA 2Division of Pediatric Hematology-Oncology-BMT, Department of Pediatrics, Medical College of Wisconsin, Milwaukee, WI, USA 3Bioinformatics Core, Blood Research Institute, Versiti, Milwaukee, WI, USA 4Divson of Hematology-Oncology, Department of Medicine, Medical College of Wisconsin, Milwaukee, WI, USA 5Department of Microbiology and Immunology, Medical College of Wisconsin, Milwaukee, WI, USA *Co-senior authors Correspondence to: Monica S. Thakar, email: [email protected] Subramaniam Malarkannan, email: [email protected] Keywords: NK cells; histone deacetylase inhibitor; Ewing sarcoma; rhabdomyosarcoma; immunotherapy Received: September 10, 2019 Accepted: March 03, 2020 Published: May 19, 2020 Copyright: Idso et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License 3.0 (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. ABSTRACT Histone deacetylase inhibitors (HDACi) are an emerging cancer therapy; however, their effect on natural killer (NK) cell-mediated anti-tumor responses remain unknown. Here, we evaluated the impact of a benzamide HDACi, entinostat, on human primary NK cells as well as tumor cell lines. Entinostat significantly upregulated the expression of NKG2D, an essential NK cell activating receptor. Independently, entinostat augmented the expression of ULBP1, HLA, and MICA/B on both rhabdomyosarcoma and Ewing sarcoma cell lines. -
IL-17-Secreting Th Cells Stat3 and Stat4 Direct Development Of
Stat3 and Stat4 Direct Development of IL-17-Secreting Th Cells Anubhav N. Mathur, Hua-Chen Chang, Dimitrios G. Zisoulis, Gretta L. Stritesky, Qing Yu, John T. O'Malley, This information is current as Reuben Kapur, David E. Levy, Geoffrey S. Kansas and Mark of September 29, 2021. H. Kaplan J Immunol 2007; 178:4901-4907; ; doi: 10.4049/jimmunol.178.8.4901 http://www.jimmunol.org/content/178/8/4901 Downloaded from References This article cites 38 articles, 15 of which you can access for free at: http://www.jimmunol.org/content/178/8/4901.full#ref-list-1 http://www.jimmunol.org/ Why The JI? Submit online. • 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 by guest on September 29, 2021 *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 © 2007 by The American Association of Immunologists All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. The Journal of Immunology Stat3 and Stat4 Direct Development of IL-17-Secreting Th Cells1 Anubhav N. Mathur,2*† Hua-Chen Chang,2*† Dimitrios G. Zisoulis,‡ Gretta L. -
Whole-Genome Cartography of Estrogen Receptor a Binding Sites
Whole-Genome Cartography of Estrogen Receptor a Binding Sites Chin-Yo Lin1[¤, Vinsensius B. Vega1[, Jane S. Thomsen1, Tao Zhang1, Say Li Kong1, Min Xie1, Kuo Ping Chiu1, Leonard Lipovich1, Daniel H. Barnett2, Fabio Stossi2, Ailing Yeo3, Joshy George1, Vladimir A. Kuznetsov1, Yew Kok Lee1, Tze Howe Charn1, Nallasivam Palanisamy1, Lance D. Miller1, Edwin Cheung1,3, Benita S. Katzenellenbogen2, Yijun Ruan1, Guillaume Bourque1, Chia-Lin Wei1, Edison T. Liu1* 1 Genome Institute of Singapore, Singapore, Republic of Singapore, 2 Department of Molecular and Integrative Physiology, University of Illinois at Urbana-Champaign, Urbana, Illinois, United States of America, 3 Department of Biochemistry, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Republic of Singapore Using a chromatin immunoprecipitation-paired end diTag cloning and sequencing strategy, we mapped estrogen receptor a (ERa) binding sites in MCF-7 breast cancer cells. We identified 1,234 high confidence binding clusters of which 94% are projected to be bona fide ERa binding regions. Only 5% of the mapped estrogen receptor binding sites are located within 5 kb upstream of the transcriptional start sites of adjacent genes, regions containing the proximal promoters, whereas vast majority of the sites are mapped to intronic or distal locations (.5 kb from 59 and 39 ends of adjacent transcript), suggesting transcriptional regulatory mechanisms over significant physical distances. Of all the identified sites, 71% harbored putative full estrogen response elements (EREs), 25% bore ERE half sites, and only 4% had no recognizable ERE sequences. Genes in the vicinity of ERa binding sites were enriched for regulation by estradiol in MCF-7 cells, and their expression profiles in patient samples segregate ERa-positive from ERa-negative breast tumors. -
Epigenetic Services Citations
Active Motif Epigenetic Services Publications The papers below contain data generated by Active Motif’s Epigenetic Services team. To learn more about our services, please give us a call or visit us at www.activemotif.com/services. Technique Target Journal Year Reference Justin C. Boucher et al. CD28 Costimulatory Domain- ATAC-Seq, Cancer Immunol. Targeted Mutations Enhance Chimeric Antigen Receptor — 2021 RNA-Seq Res. T-cell Function. Cancer Immunol. Res. doi: 10.1158/2326- 6066.CIR-20-0253. Satvik Mareedu et al. Sarcolipin haploinsufficiency Am. J. Physiol. prevents dystrophic cardiomyopathy in mdx mice. RNA-Seq — Heart Circ. 2021 Am J Physiol Heart Circ Physiol. doi: 10.1152/ Physiol. ajpheart.00601.2020. Gabi Schutzius et al. BET bromodomain inhibitors regulate Nature Chemical ChIP-Seq BRD4 2021 keratinocyte plasticity. Nat. Chem. Biol. doi: 10.1038/ Biology s41589-020-00716-z. Siyun Wang et al. cMET promotes metastasis and ChIP-qPCR FOXO3 J. Cell Physiol. 2021 epithelial-mesenchymal transition in colorectal carcinoma by repressing RKIP. J. Cell Physiol. doi: 10.1002/jcp.30142. Sonia Iyer et al. Genetically Defined Syngeneic Mouse Models of Ovarian Cancer as Tools for the Discovery of ATAC-Seq — Cancer Discovery 2021 Combination Immunotherapy. Cancer Discov. doi: doi: 10.1158/2159-8290 Vinod Krishna et al. Integration of the Transcriptome and Genome-Wide Landscape of BRD2 and BRD4 Binding BRD2, BRD4, RNA Motifs Identifies Key Superenhancer Genes and Reveals ChIP-Seq J. Immunol. 2021 Pol II the Mechanism of Bet Inhibitor Action in Rheumatoid Arthritis Synovial Fibroblasts. J. Immunol. doi: doi: 10.4049/ jimmunol.2000286. Daniel Haag et al. -
Phosphorylation of Microglial IRF5 and IRF4 by IRAK4 Regulates Inflammatory Responses to Ischemia
cells Article Phosphorylation of Microglial IRF5 and IRF4 by IRAK4 Regulates Inflammatory Responses to Ischemia Conelius Ngwa, Abdullah Al Mamun, Yan Xu, Romana Sharmeen and Fudong Liu * Department of Neurology, McGovern Medical School, The University of Texas Health Science Center at Houston, Houston, TX 77030, USA; [email protected] (C.N.); [email protected] (A.A.M.); [email protected] (Y.X.); [email protected] (R.S.) * Correspondence: [email protected]; Tel.: +1-713-500-7038; Fax: +1-713-500-0660 Abstract: Background: Interferon Regulatory Factor (IRF) 5 and 4 play a determinant role in regu- lating microglial pro- and anti-inflammatory responses to cerebral ischemia. How microglial IRF5 and IRF4 signaling are activated has been elusive. We hypothesized that interleukin-1 receptor associated kinase 4 (IRAK4) phosphorylates and activates IRF5 and IRF4 in ischemic microglia. We aimed to explore the upstream signals of the two IRFs, and to determine how the IRAK4-IRF signaling regulates the expression of inflammatory mediators, and impacts neuropathology. Meth- ods: Spontaneously Immortalized Murine (SIM)-A9 microglial cell line, primary microglia and neurons from C57BL/6 WT mice were cultured and exposed to oxygen-glucose deprivation (OGD), followed by stimulation with LPS or IL-4. An IRAK4 inhibitor (ND2158) was used to examine IRAK40s effects on the phosphorylation of IRF5/IRF4 and the impacts on neuronal morphology by co-immunoprecipitation (Co-IP)/Western blot, ELISA, and immunofluorescence assays. Results: We confirmed that IRAK4 formed a Myddosome with MyD88/IRF5/IRF4, and phosphorylated both IRFs, which subsequently translocated into the nucleus. -
Differential and Overlapping Immune Programs Regulated by IRF3 and IRF5 in Plasmacytoid Dendritic Cells
Differential and Overlapping Immune Programs Regulated by IRF3 and IRF5 in Plasmacytoid Dendritic Cells This information is current as Kwan T. Chow, Courtney Wilkins, Miwako Narita, Richard of September 28, 2021. Green, Megan Knoll, Yueh-Ming Loo and Michael Gale, Jr. J Immunol published online 8 October 2018 http://www.jimmunol.org/content/early/2018/10/05/jimmun ol.1800221 Downloaded from Supplementary http://www.jimmunol.org/content/suppl/2018/10/05/jimmunol.180022 Material 1.DCSupplemental http://www.jimmunol.org/ Why The JI? Submit online. • 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 by guest on September 28, 2021 *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 © 2018 by The American Association of Immunologists, Inc. All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. Published October 8, 2018, doi:10.4049/jimmunol.1800221 The Journal of Immunology Differential and Overlapping Immune Programs Regulated by IRF3 and IRF5 in Plasmacytoid Dendritic Cells Kwan T. Chow,*,† Courtney Wilkins,* Miwako Narita,‡ Richard Green,* Megan Knoll,* Yueh-Ming Loo,* and Michael Gale, Jr.* We examined the signaling pathways and cell type–specific responses of IFN regulatory factor (IRF) 5, an immune-regulatory transcription factor. -
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Thynn HN, Chen XF, Dong SS, Guo Y, Yang TL. Commentary: An Allele-Specific Functional SNP Associated with Two Systemic Autoimmune Diseases Modulates IRF5 Expression by Long-Range Chromatin Loop Formation. J Immunological Sci. (2020); 4(1): 6-9 Journal of Immunological Sciences Commentary Article Open Access Commentary: An Allele-Specific Functional SNP Associated with Two Systemic Autoimmune Diseases Modulates IRF5 Expression by Long- Range Chromatin Loop Formation Hlaing Nwe Thynn, Xiao-Feng Chen, Shan-Shan Dong, Yan Guo, Tie-Lin Yang* Key Laboratory of Biomedical Information Engineering of Ministry of Education, Biomedical Informatics & Genomics Center, School of Life Science and Technol- ogy, Xi’an Jiaotong University, Xi’an, Shaanxi 710049, P. R. China Systemic Lupus Erythematosus (SLE) and Systemic Sclerosis Article Info Article Notes sharing similar pathogenic features. Genetic factors play important Received: February 14, 2020 (SSc) are two typical inflammatory systemic1 autoimmune diseases Accepted: March 20, 2020 roles in the pathogenesis of both diseases . We have witnessed huge success of genome-wide association studies (GWASs) in identifying *Correspondence: hundreds of susceptibility genetic variants associated with SLE Dr. Tie-Lin Yang, Ph.D., Key Laboratory of Biomedical Information Engineering of Ministry of Education, Biomedical and SSc, however, over 90% of which are located in noncoding Informatics & Genomics Center, School of Life Science and Technology, Xi’an Jiaotong University, Xi’an, Shaanxi into biological insights towards clinical applications. Currently, 710049, P. R. China; Telephone No: 86-29-82668463; Email: regions. It is challenging and important to translate GWAS findings [email protected]. compared with traditional genetic association studies, functional studies characterizing causal functional variants and downstream © 2020 Yang TL. -
Pharmacological Activation of Estrogen Receptor Beta Augments
Pharmacological activation of estrogen receptor PNAS PLUS beta augments innate immunity to suppress cancer metastasis Linjie Zhaoa,1, Shuang Huanga,1, Shenglin Meib,1, Zhengnan Yanga, Lian Xuc, Nianxin Zhoua, Qilian Yanga, Qiuhong Shena, Wei Wangd, Xiaobing Lea, Wayne Bond Laue, Bonnie Lauf, Xin Wangd, Tao Yia, Xia Zhaoa, Yuquan Weia, Margaret Warnerg,h, Jan-Åke Gustafssong,h,2, and Shengtao Zhoua,2 aDepartment of Obstetrics and Gynecology, Key Laboratory of Birth Defects and Related Diseases of Women and Children of Ministry of Education and State Key Laboratory of Biotherapy, West China Second University Hospital, Sichuan University and Collaborative Innovation Center, 610041 Chengdu, People’s Republic of China; bShanghai Key Laboratory of Tuberculosis, Clinical Translational Research Center, Shanghai Pulmonary Hospital, Tongji University, 200433 Shanghai, People’s Republic of China; cDepartment of Pathology, West China Second Hospital of Sichuan University, 610041 Chengdu, People’sRepublicof China; dDepartment of Biomedical Sciences, City University of Hong Kong, 999077 Kowloon Tong, Hong Kong, People’sRepublicofChina;eDepartment of Emergency Medicine, Thomas Jefferson University Hospital, Philadelphia, PA 19107; fDepartment of Surgery, Emergency Medicine, Kaiser Permanente Santa Clara Medical Center (affiliate of Stanford University), Santa Clara, CA 95051; gDepartment of Biology and Biochemistry, Center for Nuclear Receptors and Cell Signaling, University of Houston, Houston, TX 77204; and hDepartment of Biosciences and Nutrition, Novum, Karolinska Institute, 14186 Stockholm, Sweden Contributed by Jan-Åke Gustafsson, March 6, 2018 (sent for review February 22, 2018; reviewed by Yunlong Lei and Haineng Xu) Metastases constitute the greatest causes of deaths from cancer. mosome 14. Both ERα and ERβ are expressed in a wide range of However, no effective therapeutic options currently exist for cancer normal tissues and cell types throughout the body. -
Estrogen Receptor-Dependent Regulation of Dendritic Cell Development and Function
REVIEW published: 10 February 2017 doi: 10.3389/fimmu.2017.00108 Estrogen Receptor-Dependent Regulation of Dendritic Cell Development and Function Sophie Laffont1*, Cyril Seillet2,3 and Jean-Charles Guéry1* 1 Centre de Physiopathologie de Toulouse Purpan (CPTP), Université de Toulouse, INSERM, CNRS, UPS, Toulouse, France, 2 Division of Molecular Immunology, The Walter and Eliza Hall Institute of Medical Research, Melbourne, VIC, Australia, 3 Department of Medical Biology, University of Melbourne, Melbourne, VIC, Australia Autoimmunity, infectious diseases and cancer affect women and men differently. Because they tend to develop more vigorous adaptive immune responses than men, women are less susceptible to some infectious diseases but also at higher risk of autoimmunity. The regulation of immune responses by sex-dependent factors probably involves several non-redundant mechanisms. A privileged area of study, however, concerns the role of sex steroid hormones in the biology of innate immune cells, especially dendritic cells (DCs). In recent years, our understanding of the lineage origin of DC populations has expanded, Edited by: and the lineage-committing transcription factors shaping peripheral DC subsets have Manfred B. Lutz, been identified. Both progenitor cells and mature DC subsets express estrogen receptors University of Würzburg, Germany (ERs), which are ligand-dependent transcription factors. This suggests that estrogens Reviewed by: may contribute to the reported sex differences in immunity by regulating DC biology. Meredith O’Keeffe, Monash University, Australia Here, we review the recent literature and highlight evidence that estrogen-dependent Pieter J. M. Leenen, activation of ERα regulates the development or the functional responses of particular DC Erasmus University Rotterdam, + Netherlands subsets.