Canonical cellular stress granules are required for arsenite-induced necroptosis mediated by Z-DNA-binding protein 1.
Canonical cellular stress granules are required for arsenite-induced necroptosis mediated by Z-DNA-binding protein 1.
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DOI：
10.1126/scisignal.abq0837
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发表时间：
2023-03-14
影响因子：
7.3
通讯作者：
中科院分区：
文献类型：
--
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细胞应激颗粒在受到应激的细胞中产生并促进细胞存活。定位于应激颗粒的细胞蛋白是Z-DNA结合蛋白1（ZBP 1），其在坏死性凋亡中起主要作用，坏死性凋亡是由激酶RIPK 3介导的程序性细胞死亡途径。在这里，我们发现应激颗粒诱导剂亚砷酸盐激活RIPK 3依赖性坏死性凋亡。该途径需要ZBP 1，其定位于亚砷酸盐诱导的应激颗粒。RIPK 3在ZBP 1存在下定位于应激颗粒，导致ZBP 1-RIPK 3坏死体的形成、RIPK 3效应物MLKL的磷酸化和坏死性凋亡的发生。没有形成应激颗粒的细胞对亚砷酸盐没有诱导坏死性凋亡。总之，这些结果表明，亚砷酸盐诱导ZBP 1介导的坏死性凋亡的方式依赖于应激颗粒的形成。
Cellular stress granules arise in cells subjected to stress and promote cell survival. A cellular protein that localizes to stress granules is Z-DNA-binding protein 1 (ZBP1), which plays a major role in necroptosis, a programmed cell death pathway mediated by the kinase RIPK3. Here, we showed that the stress-granule inducer arsenite activated RIPK3-dependent necroptosis. This pathway required ZBP1, which localized to arsenite-induced stress granules. RIPK3 localized to stress granules in the presence of ZBP1, leading to the formation of ZBP1-RIPK3 necrosomes, phosphorylation of the RIPK3 effector MLKL, and execution of necroptosis. Cells that did not form stress granules did not induce necroptosis in response to arsenite. Together, these results show that arsenite induces ZBP1-mediated necroptosis in a manner dependent on stress granule formation.
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