Despite its name, signalling induced by the tumour necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) is versatile. Besides eliciting cell death by both apoptosis and necroptosis, TRAIL can also induce migration, proliferation, and cytokine production in cancerous and non-cancerous cells. Unravelling the mechanisms regulating the intricate balance between these different outputs could therefore facilitate our understanding of the role of TRAIL in tissue homeostasis, immunity, and cancer. Ubiquitination and its reversal, deubiquitination, are crucial modulators of immune receptor signalling. This review discusses recent progress on the orchestration of TRAIL signalling outcomes by ubiquitination of various components of the signalling complexes, our understanding of the molecular switches that decide between cell death and gene activation, and what remains to be discovered.

尽管其名称，由肿瘤坏死因子（TNF）相关的凋亡诱导配体（TRAIL）诱导的信号是通用的。除了通过凋亡和坏死病引起细胞死亡外，TRAIL还可以诱导癌细胞和非癌细胞中的迁移，增殖和细胞因子产生。因此，阐明调节这些不同输出之间复杂平衡的机制可能有助于我们了解TRAIL在组织体内稳态，免疫力和癌症中的作用。泛素化及其逆转，去泛素化是免疫受体信号传导的关键调节剂。这篇综述讨论了通过信号转导复合体各种成分的泛素化对TRAIL信号转导进行编排的最新进展，