坏死性下垂
生物
细胞生物学
信号转导
背景(考古学)
程序性细胞死亡
蛋白激酶A
激酶
翻译后修饰
计算生物学
遗传学
生物化学
细胞凋亡
酶
古生物学
作者
Christopher R Horne,André L. Samson,James M. Murphy
标识
DOI:10.1016/j.tcb.2022.05.008
摘要
The past decade has seen the emergence of the necroptosis programmed cell death pathway as an important contributor to the pathophysiology of myriad diseases. The receptor interacting protein kinase (RIPK)1 and RIPK3, and the pseudokinase executioner protein, mixed lineage kinase domain-like (MLKL), have grown to prominence as the core pathway components. Depending on cellular context, these proteins also serve as integrators of signals, such as post-translational modifications and protein or metabolite interactions, adding layers of complexity to pathway regulation. Here, we describe the emerging picture of the web of proteins that tune necroptotic signal transduction and how these events have diverged across species, presumably owing to selective pressures of pathogens upon the RIPK3-MLKL protein pair.
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