Werbajh S, Nojek I, Lanz R, Costas M A
Deparmento de Cs. Biológicas, Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires, Ciudad Universitaria, Pabellón II, Argentina.
FEBS Lett. 2000 Nov 24;485(2-3):195-9. doi: 10.1016/s0014-5793(00)02223-7.
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-kappa B (NF-kappa B) transrepression. Here we report a role for the nuclear receptor coactivator RAC3, in modulating NF-kappa B transactivation. We found that RAC3 functions as a coactivator by binding to the active form of NF-kappa B and that overexpression of RAC3 restores GR-dependent transcription neglecting GR/NF-kappa B transrepression. The competition between GR and NF-kappa B for binding to RAC3 may represent a general mechanism by which both transcription factors mutually antagonize their activity.
已表明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-κB（NF-κB）的相互反式抑制作用。在此我们报告核受体辅激活因子RAC3在调节NF-κB反式激活中的作用。我们发现RAC3通过与NF-κB的活性形式结合发挥辅激活因子的功能，并且RAC3的过表达可恢复GR依赖性转录而忽略GR/NF-κB反式抑制作用。GR和NF-κB竞争与RAC3结合可能代表了这两种转录因子相互拮抗其活性的一种普遍机制。
