Department of Biochemistry, La Trobe University, Kingsbury Drive, Melbourne, Victoria 3086, Australia.
Cell Death Differ. 2010 Jan;17(1):35-45. doi: 10.1038/cdd.2009.114.
There have been a number of recent discoveries relating to the functions of inhibitors of apoptosis (IAPs) and TNF receptor-associated factors (TRAFs) in regulating signalling from TNF receptor superfamily (TNFRSF) members and some tantalizing glimpses into a wider area of influence, that of innate immune signalling. Discoveries relating to the function of these ubiquitin E3 ligases in regulating signalling from the eponymous member of the family, TNF-R1, are dealt with superbly in a separate review by Wertz and Dixit and so we will confine our discussion to the subset of the TNFRSF that does not contain a death domain (DD). In line with the available data we will divide the review into two parts, the first is restricted to the role of TRAFs 2 and 3 and cIAPs in regulating TNFRSF signalling, whereas the second will be more speculative, asking what role IAPs and TRAFs have in innate immune signalling.
最近有许多关于凋亡抑制因子 (IAPs) 和肿瘤坏死因子受体相关因子 (TRAFs) 在调节肿瘤坏死因子受体超家族 (TNFRSF) 成员信号转导方面的功能的发现，以及对更广泛的先天免疫信号转导领域的一些有趣的观察结果。关于这些泛素 E3 连接酶在调节家族中命名成员 TNF-R1 信号转导方面的功能的发现，在 Wertz 和 Dixit 的另一篇单独的综述中得到了很好的处理，因此我们将讨论仅限于不包含死亡结构域 (DD) 的 TNFRSF 亚组。根据现有数据，我们将综述分为两部分，第一部分仅限于 TRAFs 2 和 3 和 cIAPs 在调节 TNFRSF 信号转导中的作用，而第二部分更具推测性，探讨 IAPs 和 TRAFs 在先天免疫信号转导中的作用。
