Institute of Biochemistry II, Goethe University School of Medicine, Theodor-Stern-Kai 7, D-60590 Frankfurt am Main, Germany.
J Mol Cell Biol. 2011 Dec;3(6):324-6. doi: 10.1093/jmcb/mjr034. Epub 2011 Nov 23.
Recent studies have revealed that cell death stimuli can trigger programmed necrosis, necroptosis. Receptor-interacting serine-threonine kinase family RIP plays a crucial role in regulating the switch between apoptosis and necroptosis. Two studies now describe a novel RIP1 containing ~2 MDa 'Ripoptosome' complex assembled in the cytosol to mediate both apoptosis and necroptosis in response to genotoxic stress and TLR3 stimulation. Intriguingly, cIAPs and XIAP function as endogenous inhibitors of Ripoptosome by direct ubiquitination of its components.
最近的研究表明,细胞死亡刺激可以引发程序性坏死,即坏死性凋亡。受体相互作用丝氨酸/苏氨酸激酶家族 RIP 在调节细胞凋亡和坏死性凋亡之间的转换中起着关键作用。现在有两项研究描述了一种新型的 RIP1 包含约 2 MDa 的“Ripoptosome”复合物,该复合物在细胞质中组装,以响应遗传毒性应激和 TLR3 刺激来介导细胞凋亡和坏死性凋亡。有趣的是,cIAPs 和 XIAP 通过其组成部分的直接泛素化作用作为 Ripoptosome 的内源性抑制剂。