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DNA methylation and not allelic variation regulates STAT6 expression in human T cells

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dc.contributor.authorKim, Eu-Gene-
dc.contributor.authorShin, Hyun-Jin-
dc.contributor.authorLee, Chang Geun-
dc.contributor.authorPark, Hye-Young-
dc.contributor.authorPark, Heung-Woo-
dc.contributor.authorMin, Kyung-Up-
dc.contributor.authorPark, Sung-Hwan-
dc.contributor.authorLee, Chang-Woo-
dc.contributor.authorCho, Mi-La-
dc.contributor.authorCho, Sang-Heon-
dc.contributor.authorKim, Yoon-Keun-
dc.date.accessioned2012-06-27T07:03:40Z-
dc.date.available2012-06-27T07:03:40Z-
dc.date.issued2010-09-
dc.identifier.citationCLINICAL AND EXPERIMENTAL MEDICINE; Vol.10 3; 143-152ko_KR
dc.identifier.issn1591-8890-
dc.identifier.urihttps://hdl.handle.net/10371/77621-
dc.description.abstractSTAT6 transcription factor, which has been implicated in commitment to Th2, is known to be activated by IL-4 and IL-13. Accordingly, STAT6 is primarily responsible for the transcriptional effects of IL-4 and IL-13. STAT6-deficient mice are known to have defective IL-4-mediated functions, such as B cell proliferation, Th2 cell development and IgE secretion; therefore, they primarily contain the Th1 phenotype. However, the mechanism responsible for regulation of STAT6 expression transcriptionally and post-transcriptionally has yet to be elucidated. Here, we characterized the human STAT6 promoter gene and found that the transcriptional regulatory elements CCAAT and ATF were important for the STAT6 promoter activity. Direct sequencing analysis revealed that the 13 GT repeat allelic variation in noncoding exon 1 of the STAT6 gene appeared more frequently in 91 patients with asthma or rheumatoid arthritis than the 15 GT repeat variation, which is the dominant phenotype in healthy controls. However, it appears that this allelic variation did not affect the STAT6 transcriptional activity. Interestingly, treatment with a DNA methyltransferase inhibitor markedly increased the expression of STAT6 mRNA and protein in human primary T cells. In contrast, IFN-gamma treatment significantly repressed the STAT6 transcriptional activity. Therefore, the present study provides insight into the molecular basis of STAT6 expression, and in particular, demonstrates that STAT6 expression is associated with DNA hypermethylation rather than promoter polymorphisms or allelic variations.ko_KR
dc.description.sponsorshipThis work was supported by the Korea Science
and Engineering Foundation (KOSEF) [R01-2007-000-20007-0,
2008)] and KOSEF through the Rheumatism Research Center (R11-
2002-098-05003, 2008) grants funded by the Korea government.
ko_KR
dc.language.isoenko_KR
dc.publisherSPRINGERko_KR
dc.subjectSTAT6ko_KR
dc.subjectPromoter geneko_KR
dc.subjectAsthmako_KR
dc.subjectCD4+T cellsko_KR
dc.subjectDNA methylationko_KR
dc.subjectRheumatoid arthritisko_KR
dc.subjectAllelic variationko_KR
dc.titleDNA methylation and not allelic variation regulates STAT6 expression in human T cellsko_KR
dc.typeArticleko_KR
dc.contributor.AlternativeAuthor김유진-
dc.contributor.AlternativeAuthor신현진-
dc.contributor.AlternativeAuthor이창근-
dc.contributor.AlternativeAuthor박혜영-
dc.contributor.AlternativeAuthor김윤근-
dc.contributor.AlternativeAuthor박흥우-
dc.contributor.AlternativeAuthor조상헌-
dc.contributor.AlternativeAuthor민경업-
dc.contributor.AlternativeAuthor조미라-
dc.contributor.AlternativeAuthor박성환-
dc.contributor.AlternativeAuthor이창우-
dc.identifier.doi10.1007/s10238-009-0083-8-
dc.citation.journaltitleCLINICAL AND EXPERIMENTAL MEDICINE-
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College of Medicine/School of Medicine (의과대학/대학원)Internal Medicine (내과학전공)Journal Papers (저널논문_내과학전공)
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