BROWSE

Related Researcher

Author's Photo

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

ITEM VIEW & DOWNLOAD

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

Cited 15 times inthomson ciCited 17 times inthomson ci
Title
E2A/HEB and Id3 proteins control the sensitivity to glucocorticoidinduced apoptosis in thymocytes by regulating the SRG3 expression
Author
Ko, Myung GonAhn, JeongeunLee, ChangjinChung, HeekyoungJeon, SunghoChung, Hee-YSeong, Rho H
Keywords
LOOP-HELIX PROTEIN; T-CELL DEVELOPMENT; DNA-BINDING; LYMPHOCYTE DEVELOPMENT; E2A PROTEINS; SACCHAROMYCES-CEREVISIAE; TRANSCRIPTIONAL CONTROL; G(1) PROGRESSION; MAMMALIAN-CELLS; PRE-TCR
Issue Date
2004-05
Publisher
AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
Citation
JOURNAL OF BIOLOGICAL CHEMISTRY, v.279, no.21, pp.21916 - 21923
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.
URI
Go to Link
DOI
10.1074/jbc.M402145200
ISSN
0021-9258
Appears in Collections:
PHY_Journal Papers
Files in This Item:
J. Biol. Chem.-2004-Ko-21916-23.pdf Download

find_unist can give you direct access to the published full text of this article. (UNISTARs only)

Show full item record

qrcode

  • mendeley

    citeulike

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.

MENU