T Cell Receptor Signaling Inhibits Glucocorticoid-induced Apoptosis by Repressing the SRG3 Expression via Ras Activation

Ko, Myunggon; Jang, Jiho; Ahn, Jongmin; Lee, Kyuyoung; Chung, Hyun Kee; Jeon, Sung Ho; Seong, Rho Hyun

doi:10.1074/jbc.m402144200

Cited by 21 publications

(37 citation statements)

References 73 publications

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“…13,17,18 In this study, we have shown that Notch signaling directly repressed the E47-dependent SRG3 transcription (Figure 3). These results are consistent with previous reports that Notch and Deltex proteins abrogate E2A-induced transcriptional activation.…”

Section: Discussionmentioning

confidence: 51%

“…11 We have previously shown that SRG3 plays a critical role in determining the GC sensitivity in thymocytes; its expression was downregulated in mature CD4 and CD8 cells, 13 and acts as a downstream target of TCR signaling in blocking the GC-induced apoptosis. 17,18 Here, we show that Notch signaling confers developing thymocytes GC resistance also by regulating the SRG3 expression through Deltex1 blocking the recruitment of p300 coactivator to E2A/HEB. It was suggested that Notch blocks GC-induced apoptosis through the RBP-J pathway of Notch signaling.…”

Section: Discussionmentioning

confidence: 76%

“…17,18 E2A acts as a positive regulator of the SRG3 transcription and its activity is regulated by TCR signaling through Id3 induction during thymocyte maturation. Since we found two E-box elements on the promoter, E84 and E558, we tested whether E47 activates the SRG3 expression through both E-box elements.…”

Section: D2/m745mentioning

confidence: 99%

“…17 Plasmids encoding human RBP-J were generously provided by T Honjo (Koyto University, Japan). HA-tagged p300 was generously provided by Dr. Y Shi (Harvard Medical School, USA).…”

Section: Dna Constructsmentioning

confidence: 99%

“…16 We have shown that TCR signaling inhibits the SRG3 expression via Ras/MEK/ERK and PI3K pathways. 17 Id3, an inhibitor of E2A, represses the SRG3 expression by preventing E2A/HEB complex from binding to the E-box element in the SRG3 promoter and, thereby, reduces the GC sensitivity in developing thymocytes. 18 We have also reported that nitric oxide (NO) is involved in protecting immature thymocytes from the GC-induced apoptosis by repressing the SRG3 expression.…”

Section: Introductionmentioning

confidence: 99%

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Notch1 confers thymocytes a resistance to GC-induced apoptosis through Deltex1 by blocking the recruitment of p300 to the SRG3 promoter

Jang

Choi

et al. 2005

Cell Death Differ

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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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Section: Discussionmentioning

confidence: 51%

Section: Discussionmentioning

confidence: 76%

Section: D2/m745mentioning

confidence: 99%

“…17 Plasmids encoding human RBP-J were generously provided by T Honjo (Koyto University, Japan). HA-tagged p300 was generously provided by Dr. Y Shi (Harvard Medical School, USA).…”

Section: Dna Constructsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Notch1 confers thymocytes a resistance to GC-induced apoptosis through Deltex1 by blocking the recruitment of p300 to the SRG3 promoter

Jang

Choi

et al. 2005

Cell Death Differ

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1H, 15N, and 13C Resonance Assignments and Secondary Structure of the SWIRM Domain of Human BAF155, a Chromatin Remodeling Complex Componente

Moon

Shin

Lee

et al. 2013

Molecules and Cells

Self Cite

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Mammalian SWI/SNF complexes are evolutionary conserved, ATP-dependent chromatin remodeling units. BAF155 in the SWI/SNF complex contains several highly conserved domains, including SANT, SWIRM, and leucine zipper domains. The biological roles of the SWIRM domain remain unclear; however, both structural and biochemical analyses of this domain have suggested that it could mediate protein-protein or protein-DNA interactions during the chromatin remodeling process. The human BAF155 SWIRM domain was cloned into the Escherichia coli expression vector pMAL-c2X and purified using affinity chromatography for structural analysis. We report the backbone 1 H, 15 N, and 13 C resonance assignments and secondary structure of this domain using nuclear magnetic resonance (NMR) spectroscopy and the TALOS+ program. The secondary structure consists of five α-helices that form a typical histone fold for DNA interactions. Our data suggest that the BAF155 SWIRM domain interacts with nucleosome DNA (K d = 0.47 μM).

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Serum deprivation induced apoptosis in macrophage is mediated by autocrine secretion of type I IFNs

et al. 2006

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Apoptosis can be triggered by different forms of cellular stress. We here show that serum deprivation induces the expression and secretion of type I interferons and results in apoptosis in RAW 264.7 cell in a caspase dependent manner. Administration of either IFN-alpha or IFN-beta antibody partially inhibits apoptosis while the two antibodies used together totally prevents RAW264.7 cell from apoptosis. GM-CSF, but not M-CSF and IL-3, protects serum deprivation induced apoptosis. Inhibition of JAKs also prevents macrophages from apoptosis. Activation of MAPKs is not required for serum deprivation induced apoptosis. Our results are the first to demonstrate that serum deprivation-induced apoptosis acts through autocrine secretion of type I interferons.

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T Cell Receptor Signaling Inhibits Glucocorticoid-induced Apoptosis by Repressing the SRG3 Expression via Ras Activation

Abstract: Activation of T cell antigen receptor (TCR) signaling inhibits glucocorticoid (GC)-

Cited by 21 publications

References 73 publications

Notch1 confers thymocytes a resistance to GC-induced apoptosis through Deltex1 by blocking the recruitment of p300 to the SRG3 promoter

Notch1 confers thymocytes a resistance to GC-induced apoptosis through Deltex1 by blocking the recruitment of p300 to the SRG3 promoter

1H, 15N, and 13C Resonance Assignments and Secondary Structure of the SWIRM Domain of Human BAF155, a Chromatin Remodeling Complex Componente

Serum deprivation induced apoptosis in macrophage is mediated by autocrine secretion of type I IFNs

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