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Ko, Myunggon
Molecular Immunology & Cancer Epigenetics
Research Interests
  • TET proteins, DNA hydroxymethylation, oncogenesis, cancer stem cells, cancer therapy

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E2A/HEB and Id3 proteins control the sensitivity to glucocorticoidinduced apoptosis in thymocytes by regulating the SRG3 expression

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dc.contributor.author Ko, Myung Gon ko
dc.contributor.author Ahn, Jeongeun ko
dc.contributor.author Lee, Changjin ko
dc.contributor.author Chung, Heekyoung ko
dc.contributor.author Jeon, Sungho ko
dc.contributor.author Chung, Hee-Y ko
dc.contributor.author Seong, Rho H ko
dc.date.available 2015-07-27T05:04:32Z -
dc.date.created 2015-07-24 ko
dc.date.issued 2004-05 -
dc.identifier.citation JOURNAL OF BIOLOGICAL CHEMISTRY, v.279, no.21, pp.21916 - 21923 ko
dc.identifier.issn 0021-9258 ko
dc.identifier.uri https://scholarworks.unist.ac.kr/handle/201301/12657 -
dc.identifier.uri http://www.jbc.org/content/279/21/21916.long ko
dc.description.abstract The E protein family transcription factors encoded by the E2A and HEB genes are known to play critical roles in the coordinate regulation of lymphocyte development. Previous studies have shown that T cell receptor (TCR) signals rapidly induce Id3, a dominant negative antagonist of E2A activity and allow thymocytes to survive selection events in the thymus. Here we show that SRG3 acts as a novel downstream target of E2A/HeLa E box-binding (HEB) complex and modulates glucocorticoid (GC) susceptibility in thymocytes in response to TCR signals. We have identified a putative E box element in the SRG3 promoter that is required for optimal promoter activity. The transcription factors E2A and HEB specifically associate with the E box element. Moreover, E2A-HEB heterodimers cooperated to activate SRG3 transcription, which was inhibited by the expression of Id proteins. TCR-mediated signals rapidly induced Id3 via MEK/ERK activation and thereby kept the E2A/HEB complex from binding to the E box element in the SRG3 promoter. Retroviral transduction of Id3 also repressed the SRG3 expression by inhibiting the E box binding activity of the E2A/HEB complex. Intriguingly, enforced Id3 expression conferred thymocyte resistance to GCs, which could be overcome by the overexpression of SRG3. Taken together, these results suggest that Id3 may enhance the viability of immature thymocytes by at least rendering them resistant to GCs through SRG3 down-regulation. ko
dc.description.statementofresponsibility close -
dc.language ENG ko
dc.publisher AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC ko
dc.subject LOOP-HELIX PROTEIN ko
dc.subject T-CELL DEVELOPMENT ko
dc.subject DNA-BINDING ko
dc.subject LYMPHOCYTE DEVELOPMENT ko
dc.subject E2A PROTEINS ko
dc.subject SACCHAROMYCES-CEREVISIAE ko
dc.subject TRANSCRIPTIONAL CONTROL ko
dc.subject G(1) PROGRESSION ko
dc.subject MAMMALIAN-CELLS ko
dc.subject PRE-TCR ko
dc.title E2A/HEB and Id3 proteins control the sensitivity to glucocorticoidinduced apoptosis in thymocytes by regulating the SRG3 expression ko
dc.type ARTICLE ko
dc.identifier.scopusid 2-s2.0-2542461044 ko
dc.identifier.wosid 000221417100031 ko
dc.type.rims ART ko
dc.description.wostc 15 *
dc.description.scopustc 17 *
dc.date.tcdate 2015-12-28 *
dc.date.scptcdate 2015-11-04 *
dc.identifier.doi 10.1074/jbc.M402145200 ko
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