Yin-Yang 1 and Yin-Yang 2 exert opposing effects on the promoter activity of interleukin 4
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Lee, Sung Ho | - |
dc.contributor.author | Cho, Young-Chang | - |
dc.contributor.author | Jeong, Hyung Min | - |
dc.contributor.author | Kim, Kyung Hee | - |
dc.contributor.author | Choi, Hyun Jin | - |
dc.contributor.author | Lee, Kwang Youl | - |
dc.contributor.author | Kang, Bok Yun | - |
dc.date.accessioned | 2023-03-08T17:46:01Z | - |
dc.date.available | 2023-03-08T17:46:01Z | - |
dc.date.issued | 2016-04 | - |
dc.identifier.issn | 0253-6269 | - |
dc.identifier.issn | 1976-3786 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/64284 | - |
dc.description.abstract | Interleukin (IL)-4 acts on T cells as a growth and activation factor, and promotes the differentiation of type 2 T helper cells. In T cells, expression of the gene encoding IL-4 is regulated by inducible or constitutive factors. Yin-Yang (YY)-1 is one of constitutive transcription factors binding to the IL-4 promoter. The recently identified YY2 protein is similar to YY1, with both sharing high levels of homology in their zinc finger motifs. However, the role of YY2 in T cells is unclear. YY1 and YY2 were constitutively expressed in EL4 T cells, and their expression was not dependent on stimulation. IL-4 promoter (-741/+56 fragment) activity was enhanced by YY1, but inhibited by YY2. The enhanced IL-4 promoter activity by YY1 was reduced by simultaneous expression of YY2. In addition, the DNA binding affinity of YY1 to the IL-4 promoter was adversely affected by YY2. Our results suggest that YY1 and YY2 exert opposing effects on the IL-4 promoter as they compete for the same DNA binding sites. | - |
dc.format.extent | 8 | - |
dc.language | 영어 | - |
dc.language.iso | ENG | - |
dc.publisher | PHARMACEUTICAL SOC KOREA | - |
dc.title | Yin-Yang 1 and Yin-Yang 2 exert opposing effects on the promoter activity of interleukin 4 | - |
dc.type | Article | - |
dc.identifier.doi | 10.1007/s12272-015-0622-7 | - |
dc.identifier.bibliographicCitation | ARCHIVES OF PHARMACAL RESEARCH, v.39, no.4, pp 547 - 554 | - |
dc.identifier.kciid | ART002100096 | - |
dc.description.isOpenAccess | N | - |
dc.identifier.wosid | 000374297100012 | - |
dc.identifier.scopusid | 2-s2.0-84940951091 | - |
dc.citation.endPage | 554 | - |
dc.citation.number | 4 | - |
dc.citation.startPage | 547 | - |
dc.citation.title | ARCHIVES OF PHARMACAL RESEARCH | - |
dc.citation.volume | 39 | - |
dc.type.docType | Article | - |
dc.publisher.location | 대한민국 | - |
dc.subject.keywordAuthor | YY1 | - |
dc.subject.keywordAuthor | YY2 | - |
dc.subject.keywordAuthor | IL-4 | - |
dc.subject.keywordAuthor | Th2 cell | - |
dc.subject.keywordAuthor | Constitutive factor | - |
dc.subject.keywordPlus | TRANSCRIPTION FACTOR YY1 | - |
dc.subject.keywordPlus | ACTIVATED T-CELLS | - |
dc.subject.keywordPlus | NUCLEAR FACTOR | - |
dc.subject.keywordPlus | GENE-EXPRESSION | - |
dc.subject.keywordPlus | FACTOR YIN-YANG-1 | - |
dc.subject.keywordPlus | BINDING PROTEIN | - |
dc.subject.keywordPlus | GAMMA PROMOTER | - |
dc.subject.keywordPlus | IL-4 | - |
dc.subject.keywordPlus | MECHANISMS | - |
dc.subject.keywordPlus | REPRESSION | - |
dc.relation.journalResearchArea | Pharmacology & Pharmacy | - |
dc.relation.journalWebOfScienceCategory | Chemistry, Medicinal | - |
dc.relation.journalWebOfScienceCategory | Pharmacology & Pharmacy | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.description.journalRegisteredClass | kci | - |
Items in ScholarWorks are protected by copyright, with all rights reserved, unless otherwise indicated.
84, Heukseok-ro, Dongjak-gu, Seoul, Republic of Korea (06974)02-820-6194
COPYRIGHT 2019 Chung-Ang University All Rights Reserved.
Certain data included herein are derived from the © Web of Science of Clarivate Analytics. All rights reserved.
You may not copy or re-distribute this material in whole or in part without the prior written consent of Clarivate Analytics.