Notch1 confers thymocytes a resistance to GC-induced apoptosis through Deltex1 by blocking the recruitment of p300 to the SRG3 promoteropen access
- Authors
- Jang, Jiho; Choi, Young Il; Choi, Jinwook; Lee, Kyoo-Yung; Chung, Heekyoung; Jeon, Seong-Hyun; Seong, Rho Hyun
- Issue Date
- Sep-2006
- Publisher
- NATURE PUBLISHING GROUP
- Keywords
- Notch; Deltex1; RBP-J; p300; E2A; HEB; SRG3; glucocorticoid
- Citation
- CELL DEATH AND DIFFERENTIATION, v.13, no.9, pp.1495 - 1505
- Indexed
- SCIE
SCOPUS
- Journal Title
- CELL DEATH AND DIFFERENTIATION
- Volume
- 13
- Number
- 9
- Start Page
- 1495
- End Page
- 1505
- URI
- https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/181054
- DOI
- 10.1038/sj.cdd.4401827
- ISSN
- 1350-9047
- Abstract
- One notable phenotypic change during the differentiation of immature thymocytes into either mature CD4 or CD8 singlepositive lineages is the acquisition of a resistance to glucocorticoid (GC)-induced apoptosis. We have previously reported that SRG3 is critical in determining the sensitivity for the GC-induced apoptosis in developing thymocytes. We report here that Notch signaling downregulates the transcriptional activation of SRG3 through N-box and/or E-box elements on its promoter. RBP-J represses SRG3 transcription through the N-box motif. On the other hand, Deltex1 competitively inhibits the binding of p300 to E2A/HEB protein bound to the E-box elements and represses the SRG3 promoter activity. Moreover, enforced expression of Deltex1 restored double- positive (DP) thymocyte survival from the GC-induced apoptosis. Our results suggest that Notch signaling confers differentiating DP thymocytes resistance to GCs by regulating the SRG3 expression through Deltex1, and that Deltex1 and SRG3 may play a significant role during DP thymocyte maturation.
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