Max Delbrück Center for Molecular Medicine, Berlin, Germany.
Immunol Rev. 2012 Mar;246(1):59-76. doi: 10.1111/j.1600-065X.2012.01102.x.
The inhibitory IκB proteins have been discovered as fundamental regulators of the inducible transcription factor nuclear factor-κB (NF-κB). As a generally excepted model, stimulus-dependent destruction of inhibitory IκBs and processing of precursor molecules, both promoted by components of the signal integrating IκB kinase complex, are the key events for the release of various NF-κB/Rel dimers and subsequent transcriptional activation. Intense research of more than 20 years provides evidence that the extending family of IκBs act not simply as reversible inhibitors of NF-κB activation but rather as a complex regulatory module, which assures feedback regulation of the NF-κB system and either can inhibit or promote transcriptional activity in a stimulus-dependent manner. Thus, IκB and NF-κB/Rel family proteins establish a complex interrelationship that allows modulated NF-κB-dependent transcription, tailored to the physiological environment.
抑制性 IκB 蛋白已被发现是诱导型转录因子核因子-κB（NF-κB）的基本调节因子。作为一个普遍接受的模型，刺激依赖性抑制性 IκB 的破坏和前体分子的加工，这两者都由信号整合 IκB 激酶复合物的成分促进，是释放各种 NF-κB/Rel 二聚体和随后转录激活的关键事件。20 多年的深入研究提供了证据，证明 IκB 的扩展家族不仅作为 NF-κB 激活的可逆抑制剂起作用，而是作为一个复杂的调节模块，确保 NF-κB 系统的反馈调节，并且可以以刺激依赖性的方式抑制或促进转录活性。因此，IκB 和 NF-κB/Rel 家族蛋白建立了一种复杂的相互关系，允许调节 NF-κB 依赖性转录，以适应生理环境。
