从炎症到细胞死亡的转变。
Flipping the Switch from Inflammation to Cell Death.
机构信息
Graduate Program in Genetics, Tufts Graduate School of Biomedical Sciences, Boston, MA 02111, USA.
Graduate Program in Genetics, Tufts Graduate School of Biomedical Sciences, Boston, MA 02111, USA; Department of Immunology, Tufts University School of Medicine, Boston, MA 02111, USA; Petrozavodsk State University, Petrozavodsk, Republic of Karelia 185910, Russia.
出版信息
Trends Immunol. 2020 Aug;41(8):648-651. doi: 10.1016/j.it.2020.06.007. Epub 2020 Jul 1.
Abstract
Multiple research groups have demonstrated that caspase-8 (CASP8)-mediated gasdermin D (GSDMD) cleavage drives pyroptotic cell death. Here, we discuss a novel role for the enzymatically inactive homolog of CASP8, the long isoform of cellular FLICE-like inhibitory protein (cFLIP), in the regulation of this process. Specifically, cFLIP-deficiency provides a model in which to study the mechanisms regulating CASP8-mediated activation of cell death and inflammatory signaling.
摘要
多个研究小组已经证明，半胱氨酸天冬氨酸蛋白酶-8（CASP8）介导的 Gasdermin D（GSDMD）裂解驱动细胞焦亡。在这里，我们讨论了 CASP8 的无酶活性同源物，即细胞型 Fas 相关死亡域抑制蛋白（cFLIP）的长亚型在调节这一过程中的新作用。具体来说，cFLIP 缺陷提供了一个模型，可以用来研究调节 CASP8 介导的细胞死亡和炎症信号激活的机制。
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本文引用的文献
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Science. 2020 Mar 20;367(6484):1379-1384. doi: 10.1126/science.aay3878.
2
Innate immune priming in the absence of TAK1 drives RIPK1 kinase activity-independent pyroptosis, apoptosis, necroptosis, and inflammatory disease.在不存在 TAK1 的情况下，先天免疫引发 RIPK1 激酶活性非依赖性细胞焦亡、细胞凋亡、坏死性凋亡和炎症性疾病。
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