Transcription Factors Oct-1 and GATA-3 Cooperatively Regulate Th2 Cytokine Gene Expression via the RHS5 within the Th2 Locus Control Region
The T helper type 2 (Th2) locus control region (LCR) regulates Th2 cell differentiation. Several transcription factors bind to the LCR to modulate the expression of Th2 cytokine genes, but the molecular mechanisms behind Th2 cytokine gene regulation are incompletely understood. Here, we used databas...
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| description | The T helper type 2 (Th2) locus control region (LCR) regulates Th2 cell differentiation. Several transcription factors bind to the LCR to modulate the expression of Th2 cytokine genes, but the molecular mechanisms behind Th2 cytokine gene regulation are incompletely understood. Here, we used database analysis and an oligonucleotide competition/electrophoretic mobility shift assays to search for transcription factors binding to RHS5, a DNase I hypersensitive site (DHS) within the Th2 LCR. Consequently, we demonstrated that GATA-binding protein-3 (GATA-3), E26 transformation-specific protein 1 (Ets-1), octamer transcription factor-1 (Oct-1), and Oct-2 selectively associate with RHS5. Furthermore, chromatin immunoprecipitation and luciferase reporter assays showed that Oct-1 and Oct-2 bound within the Il4 promoter region and the Th2 LCR, and that Oct-1 and GATA-3 or Oct-2 synergistically triggered the transactivational activity of the Il4 promoter through RHS5. These results suggest that Oct-1 and GATA-3/Oct-2 direct Th2 cytokine gene expression in a cooperative manner. |
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Several transcription factors bind to the LCR to modulate the expression of Th2 cytokine genes, but the molecular mechanisms behind Th2 cytokine gene regulation are incompletely understood. Here, we used database analysis and an oligonucleotide competition/electrophoretic mobility shift assays to search for transcription factors binding to RHS5, a DNase I hypersensitive site (DHS) within the Th2 LCR. Consequently, we demonstrated that GATA-binding protein-3 (GATA-3), E26 transformation-specific protein 1 (Ets-1), octamer transcription factor-1 (Oct-1), and Oct-2 selectively associate with RHS5. Furthermore, chromatin immunoprecipitation and luciferase reporter assays showed that Oct-1 and Oct-2 bound within the Il4 promoter region and the Th2 LCR, and that Oct-1 and GATA-3 or Oct-2 synergistically triggered the transactivational activity of the Il4 promoter through RHS5. These results suggest that Oct-1 and GATA-3/Oct-2 direct Th2 cytokine gene expression in a cooperative manner.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0148576</identifier><identifier>PMID: 26840450</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Analysis ; Animals ; Biology and Life Sciences ; Cell differentiation ; Cell Line ; Chromatin ; Cytokines ; Deoxyribonuclease ; Electrophoretic mobility ; Epigenetics ; ETS protein ; GATA-3 protein ; GATA-binding protein ; GATA3 Transcription Factor - genetics ; GATA3 Transcription Factor - metabolism ; Gene expression ; Gene Expression Regulation - physiology ; Gene regulation ; Genetic aspects ; Genetic regulation ; Genetic transformation ; Helper cells ; Immunology ; Immunoprecipitation ; Interleukin 4 ; Interleukin-4 - biosynthesis ; Interleukin-4 - genetics ; Life sciences ; Locus Control Region - physiology ; Lymphocytes ; Lymphocytes T ; Medical research ; Medicine and Health Sciences ; Mice ; Molecular modelling ; Oct-1 protein ; Octamer Transcription Factor-1 - genetics ; Octamer Transcription Factor-1 - metabolism ; Oligonucleotides ; Organic Cation Transport Proteins - genetics ; Organic Cation Transport Proteins - metabolism ; Organic Cation Transporter 2 ; Penicillin ; Physical Sciences ; Physiological aspects ; Proteins ; Research and Analysis Methods ; Rodents ; T cell receptors ; Th2 Cells - cytology ; Th2 Cells - metabolism ; Transcription factors ; Transformation ; Transgenic animals</subject><ispartof>PloS one, 2016-02, Vol.11 (2), p.e0148576-e0148576</ispartof><rights>COPYRIGHT 2016 Public Library of Science</rights><rights>2016 Kim et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2016 Kim et al 2016 Kim et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c692t-3cdf3fcc6d8d1dbe0119b0f8c4150a2a52767ab331c90024df89f875eb1eeb573</citedby><cites>FETCH-LOGICAL-c692t-3cdf3fcc6d8d1dbe0119b0f8c4150a2a52767ab331c90024df89f875eb1eeb573</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4740509/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4740509/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,2102,2928,23866,27924,27925,53791,53793,79600,79601</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26840450$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Das, Gobardhan</contributor><creatorcontrib>Kim, Kiwan</creatorcontrib><creatorcontrib>Kim, Najung</creatorcontrib><creatorcontrib>Lee, Gap Ryol</creatorcontrib><title>Transcription Factors Oct-1 and GATA-3 Cooperatively Regulate Th2 Cytokine Gene Expression via the RHS5 within the Th2 Locus Control Region</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>The T helper type 2 (Th2) locus control region (LCR) regulates Th2 cell differentiation. Several transcription factors bind to the LCR to modulate the expression of Th2 cytokine genes, but the molecular mechanisms behind Th2 cytokine gene regulation are incompletely understood. Here, we used database analysis and an oligonucleotide competition/electrophoretic mobility shift assays to search for transcription factors binding to RHS5, a DNase I hypersensitive site (DHS) within the Th2 LCR. Consequently, we demonstrated that GATA-binding protein-3 (GATA-3), E26 transformation-specific protein 1 (Ets-1), octamer transcription factor-1 (Oct-1), and Oct-2 selectively associate with RHS5. Furthermore, chromatin immunoprecipitation and luciferase reporter assays showed that Oct-1 and Oct-2 bound within the Il4 promoter region and the Th2 LCR, and that Oct-1 and GATA-3 or Oct-2 synergistically triggered the transactivational activity of the Il4 promoter through RHS5. These results suggest that Oct-1 and GATA-3/Oct-2 direct Th2 cytokine gene expression in a cooperative manner.</description><subject>Analysis</subject><subject>Animals</subject><subject>Biology and Life Sciences</subject><subject>Cell differentiation</subject><subject>Cell Line</subject><subject>Chromatin</subject><subject>Cytokines</subject><subject>Deoxyribonuclease</subject><subject>Electrophoretic mobility</subject><subject>Epigenetics</subject><subject>ETS protein</subject><subject>GATA-3 protein</subject><subject>GATA-binding protein</subject><subject>GATA3 Transcription Factor - genetics</subject><subject>GATA3 Transcription Factor - metabolism</subject><subject>Gene expression</subject><subject>Gene Expression Regulation - physiology</subject><subject>Gene regulation</subject><subject>Genetic aspects</subject><subject>Genetic regulation</subject><subject>Genetic transformation</subject><subject>Helper cells</subject><subject>Immunology</subject><subject>Immunoprecipitation</subject><subject>Interleukin 4</subject><subject>Interleukin-4 - 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genetics</topic><topic>GATA3 Transcription Factor - metabolism</topic><topic>Gene expression</topic><topic>Gene Expression Regulation - physiology</topic><topic>Gene regulation</topic><topic>Genetic aspects</topic><topic>Genetic regulation</topic><topic>Genetic transformation</topic><topic>Helper cells</topic><topic>Immunology</topic><topic>Immunoprecipitation</topic><topic>Interleukin 4</topic><topic>Interleukin-4 - biosynthesis</topic><topic>Interleukin-4 - genetics</topic><topic>Life sciences</topic><topic>Locus Control Region - physiology</topic><topic>Lymphocytes</topic><topic>Lymphocytes T</topic><topic>Medical research</topic><topic>Medicine and Health Sciences</topic><topic>Mice</topic><topic>Molecular modelling</topic><topic>Oct-1 protein</topic><topic>Octamer Transcription Factor-1 - genetics</topic><topic>Octamer Transcription Factor-1 - metabolism</topic><topic>Oligonucleotides</topic><topic>Organic Cation Transport Proteins - genetics</topic><topic>Organic Cation Transport Proteins - metabolism</topic><topic>Organic Cation Transporter 2</topic><topic>Penicillin</topic><topic>Physical Sciences</topic><topic>Physiological aspects</topic><topic>Proteins</topic><topic>Research and Analysis Methods</topic><topic>Rodents</topic><topic>T cell receptors</topic><topic>Th2 Cells - cytology</topic><topic>Th2 Cells - metabolism</topic><topic>Transcription factors</topic><topic>Transformation</topic><topic>Transgenic animals</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kim, Kiwan</creatorcontrib><creatorcontrib>Kim, Najung</creatorcontrib><creatorcontrib>Lee, Gap Ryol</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Opposing Viewpoints</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Proquest Nursing & Allied Health Source</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Meteorological & Geoastrophysical Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Agricultural Science Collection</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Materials Science & Engineering Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>Advanced Technologies & Aerospace Collection</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Materials Science Collection</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Materials Science Database</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Meteorological & Geoastrophysical Abstracts - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kim, Kiwan</au><au>Kim, Najung</au><au>Lee, Gap Ryol</au><au>Das, Gobardhan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Transcription Factors Oct-1 and GATA-3 Cooperatively Regulate Th2 Cytokine Gene Expression via the RHS5 within the Th2 Locus Control Region</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2016-02-03</date><risdate>2016</risdate><volume>11</volume><issue>2</issue><spage>e0148576</spage><epage>e0148576</epage><pages>e0148576-e0148576</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>The T helper type 2 (Th2) locus control region (LCR) regulates Th2 cell differentiation. Several transcription factors bind to the LCR to modulate the expression of Th2 cytokine genes, but the molecular mechanisms behind Th2 cytokine gene regulation are incompletely understood. Here, we used database analysis and an oligonucleotide competition/electrophoretic mobility shift assays to search for transcription factors binding to RHS5, a DNase I hypersensitive site (DHS) within the Th2 LCR. Consequently, we demonstrated that GATA-binding protein-3 (GATA-3), E26 transformation-specific protein 1 (Ets-1), octamer transcription factor-1 (Oct-1), and Oct-2 selectively associate with RHS5. Furthermore, chromatin immunoprecipitation and luciferase reporter assays showed that Oct-1 and Oct-2 bound within the Il4 promoter region and the Th2 LCR, and that Oct-1 and GATA-3 or Oct-2 synergistically triggered the transactivational activity of the Il4 promoter through RHS5. These results suggest that Oct-1 and GATA-3/Oct-2 direct Th2 cytokine gene expression in a cooperative manner.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>26840450</pmid><doi>10.1371/journal.pone.0148576</doi><oa>free_for_read</oa></addata></record> |
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| subjects | Analysis Animals Biology and Life Sciences Cell differentiation Cell Line Chromatin Cytokines Deoxyribonuclease Electrophoretic mobility Epigenetics ETS protein GATA-3 protein GATA-binding protein GATA3 Transcription Factor - genetics GATA3 Transcription Factor - metabolism Gene expression Gene Expression Regulation - physiology Gene regulation Genetic aspects Genetic regulation Genetic transformation Helper cells Immunology Immunoprecipitation Interleukin 4 Interleukin-4 - biosynthesis Interleukin-4 - genetics Life sciences Locus Control Region - physiology Lymphocytes Lymphocytes T Medical research Medicine and Health Sciences Mice Molecular modelling Oct-1 protein Octamer Transcription Factor-1 - genetics Octamer Transcription Factor-1 - metabolism Oligonucleotides Organic Cation Transport Proteins - genetics Organic Cation Transport Proteins - metabolism Organic Cation Transporter 2 Penicillin Physical Sciences Physiological aspects Proteins Research and Analysis Methods Rodents T cell receptors Th2 Cells - cytology Th2 Cells - metabolism Transcription factors Transformation Transgenic animals |
| title | Transcription Factors Oct-1 and GATA-3 Cooperatively Regulate Th2 Cytokine Gene Expression via the RHS5 within the Th2 Locus Control Region |
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