RAC-3 is a NF-κB coactivator
RAC-3 is a NF-κB coactivator
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DOI：
10.1016/s0014-5793(00)02223-7
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发表时间：
2000-11-24
期刊：
影响因子：
3.5
通讯作者：
Costas, MA
中科院分区：
文献类型：
--
作者：
Werbajh, S;Nojek, I;Costas, MA
细胞因子和糖皮质激素相互拮抗其功能的分子机制涉及糖皮质激素受体（GR）/核因子-κ B（NF-κ B）的相互反式抑制。我们发现RAC 3通过与NF-κ B的活性形式结合而起共激活剂的作用，并且RAC 3的过表达恢复GR依赖的转录，而忽略GR/NF-κ B的反式抑制。GR和NF-κ B之间竞争结合RAC 3可能代表了两种转录因子相互拮抗其活性的一般机制。(C)2000年欧洲生物化学学会联合会。由Elsevier Science B. V.出版，版权所有。
It has been shown that the molecular mechanism by which cytokines and glucocorticoids mutually antagonize their functions involves a mutual glucocorticoid receptor (GR)/nuclear factor-kappaB (NF-kappaB) transrepression, Here we report a role for the nuclear receptor coactivator RAC3, in modulating NF-kappaB transactivation. We found that RAC3 functions as a coactivator by binding to the active form of NF-kappaB and that overexpression of RAC3 restores GR-dependent transcription neglecting GR/NF-kappaB transrepression, The competition between GR and NF-kappaB for binding to RAC3 may represent a general mechanism by which both transcription factors mutually antagonize their activity. (C) 2000 Federation of European Biochemical Societies. Published by Elsevier Science B.V. All rights reserved.