The transcription factor nuclear factor-kappaB (NF-kappaB) has a pivotal role in initiating inflammation and raising an effective immune response. Because NF-kappaB activation depends on ubiquitination, cells have developed ubiquitin (Ub)-mediated strategies for inhibiting NF-kappaB activation and preventing excessive inflammation. Recent findings concerning tumor necrosis factor (TNF) receptor and toll-like receptor (TLR)-interleukin-1 (IL-1) receptor signalling pathways show that Ub can be a tool as well as a target for NF-kappaB inhibitory proteins, either by labelling specific signalling proteins for proteasome-dependent degradation or by serving as a target for specific de-ubiquitinating enzymes that prevent the formation of pertinent signalling complexes. Interfering with ubiquitination therefore seems to be a versatile means for regulating NF-kappaB activity, indicating that studies of Ub-mediated signalling might hold the key for developing new therapeutic strategies for inflammatory disease.

译文

转录因子核因子-κB(NF-kappaB)在引发炎症和提高有效免疫反应方面具有关键作用。由于NF-κB的活化依赖于泛素化,因此细胞已开发出由泛素(Ub)介导的抑制NF-κB活化和防止过度炎症的策略。有关肿瘤坏死因子(TNF)受体和toll样受体(TLR)-白介素1(IL-1)受体信号通路的最新发现表明,Ub既可以作为NF-κB抑制蛋白的工具,也可以作为靶标。通过为蛋白酶体依赖性降解标记特定的信号蛋白,或作为防止相关信号复合物形成的特定去泛素化酶的靶标。因此,干扰泛素化似乎是调节NF-κB活性的通用手段,这表明对Ub介导的信号传导的研究可能是开发炎症性疾病新治疗策略的关键。

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