The glucocorticoid receptor and STAT6 physically and functionally interact in T-lymphocytes
The glucocorticoid receptor and STAT6 physically and functionally interact in T-lymphocytes
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DOI：
10.1016/s0014-5793(00)02297-3
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发表时间：
2000-12-29
期刊：
影响因子：
3.5
通讯作者：
Pallardy, M
中科院分区：
文献类型：
--
作者：
Biola, A;Andréau, K;Pallardy, M
在淋巴细胞中，糖皮质激素 (GC) 和白细胞介素 4 信号通路已知会相互作用，地塞米松抑制 IL-4 介导的增殖或 IL-4 抑制 GC 诱导的细胞凋亡就证明了这一点。在这项研究中，我们描述了这种相互干扰的分子基础，我们报告说，在小鼠 CTLL-2 细胞中，IL-4 抑制 GC 诱导的 MMTV（小鼠乳腺肿瘤病毒）启动子反式激活，并且 GC 抑制 IL-4 诱导的 STAT6（信号转导子和转录激活子 6）响应启动子的反式激活，而不影响 IL-4 刺激的 STAT6 DNA 结合。此外，我们证明了 GC 受体和 STAT6 之间的物理关联，这被证明是功能相关的，因为 STAT6 过表达增加了 IL-4 对 GC 诱导的 MMTV 反式激活的抑制作用。 (C) 2000 年欧洲生化学会联合会。由 Elsevier Science B.V. 出版。保留所有权利。
In lymphocytes, glucocorticoids (GC)- and interleukin-4-signaling pathways are known to interact, as evidenced by inhibition of IL-4-mediated proliferation by dexamethasone or suppression of GC-induced apoptosis by IL-4, Tn this study, we characterized the molecular basis for this reciprocal interference, We report that, in murine CTLL-2 cells, IL-4 inhibits GC-induced MMTV (mouse mammary tumor virus) promoter transactivation, and that GC suppress IL-4-induced transactivation of a STAT6 (signal transducers and activators of transcription 6)-responsive promoter without affecting IL-4-stimulated STAT6 DNA-binding. Moreover, we evidenced a physical association between GC receptor and STAT6, which proved to be functionally relevant, since STAT6 overexpression increased the IL-4 inhibitory effect on GC-induced MMTV transactivation. (C) 2000 Federation of European Biochemical Societies. Published by Elsevier Science B.V. All rights reserved.