作者发现:(1)在围产期,缺失酶活性的caspase-8(Casp8C362A/C362A)具有诱导细胞死亡的功能,而这一功能并不依赖于NLRP3,FADD和RIPK1,也就是说,并不依赖于炎症小体活化和细胞凋亡途径;(2)对于参与细胞焦亡通路(pyroptotic cell death)的两种蛋白酶caspase-1和caspase-11,caspase-1是Casp8C362A/C362AMlkl−...
作者发现:(1)在围产期,缺失酶活性的caspase-8(Casp8C362A/C362A)具有诱导细胞死亡的功能,而这一功能并不依赖于NLRP3,FADD和RIPK1,也就是说,并不依赖于炎症小体活化和细胞凋亡途径;(2)对于参与细胞焦亡通路(pyroptotic cell death)的两种蛋白酶caspase-1和caspase-11,caspase-1是Casp8C362A/C362AMlkl−...
参考文献:[1] Van Opdenbosch, Nina., Lamkanfi, Mohamed.. Caspases in Cell Death, Inflammation, and Disease. Immunity, 2019, 50(6):1352-1364.[2] Horn, Sebastian., Hughes, Michelle A., Schilling, Ramon., Sticht, Carsten., Tenev, Tencho.. Caspase-10 Negatively Regulates Caspase-8-Me...
[1] Van Opdenbosch, Nina., Lamkanfi, Mohamed.. Caspases in Cell Death, Inflammation, and Disease. Immunity, 2019, 50(6):1352-1364. [2] Horn, Sebastian., Hughes, Michelle A., Schilling, Ramon., Sticht, Carsten., Tenev, Tencho.. Caspase-10 Negatively Regulates Caspase-8-Mediated Cel...
近日,这项研究发表在《Immunity》上,题为“Interferon-γ primes macrophages for pathogen ligand-induced killing via a caspase-8 and mitochondrial cell death pathway”,指出了具有创造出阻断Caspase-8和一氧化氮的药物的潜力,以防止这种新的炎症细胞死亡过程。操控这一细胞死亡途径可以为患有炎症性疾病的患者带来...
【学术前沿】韩家淮/莫玮合作揭示解除Caspase-8对Necroptosis抑制作用的内源性机制 坏死样凋亡(Necroptosis)是一种由RIP3-MLKL介导的程序性细胞坏死(programmed necrosis),它可以被Death receptors, TLR receptors, Interferon receptor以及病原体感染等多种刺激所诱发。坏死样凋亡伴随着细胞内容物的释放,它在TNF介导的...
cell deathCaspase-8, a well-characterized initiator of apoptosis, has also been found to play non-apoptotic roles in cells. In this study, we reveal that caspase-8 can induce cell death in a special way, which does not depend on activation of caspases and mitochondrial initiation. Instead, ...
Caspase-8决定细胞死亡的不同方式 近日,来自美国基因泰克公司Vishva M. Dixit和Kim Newton研究团队在《Nature》杂志上发表了标题为“Activity of caspase-8 determines plasticity between cell death pathways”的研究成果,发现caspase-8的活性决定了细胞死亡途径之间的可塑性。
2024年4月27日,北京生命科学研究所/清华大学生物医学交叉研究院邵峰团队在Protein & Cell杂志在线发表题为"Dissecting caspase-2-mediated cell death: from intrinsic PIDDosome activation to chemical modulation"的研究论文,证明了由PIDDosome激活的caspase-2可以直接切割BID分子,激活下游的线粒体内源凋亡通路。此外...
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