The RIP3-RIP1-NF-κB signaling axis is dispensable for necroptotic cells to elicit cross-priming of CD8 T cells.
作者信息
Ren Junming, Jia Xian, Zhao Yihao, Shi Wenke, Lu Jiongcong, Zhang Yingying, Wu Jianfeng, Liang Bo, Wu Rui, Fu Guo, Han Jiahuai
机构信息
State Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Signaling Network, School of Life Sciences, Xiamen University, Xiamen Fujian 361005, China.
出版信息
Cell Mol Immunol. 2017 Jul;14(7):639-642. doi: 10.1038/cmi.2017.31. Epub 2017 Jun 19.
Abstract
摘要
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The RIP3-RIP1-NF-κB signaling axis is dispensable for necroptotic cells to elicit cross-priming of CD8 T cells.RIP3-RIP1-NF-κB信号轴对于坏死性凋亡细胞引发CD8 T细胞的交叉启动并非必需。
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本文引用的文献
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Vaccination with Necroptotic Cancer Cells Induces Efficient Anti-tumor Immunity.用坏死性癌细胞进行疫苗接种可诱导有效的抗肿瘤免疫。
Cell Rep. 2016 Apr 12;15(2):274-87. doi: 10.1016/j.celrep.2016.03.037. Epub 2016 Mar 31.
2
RIPK1 and NF-κB signaling in dying cells determines cross-priming of CD8⁺ T cells.死亡细胞中的RIPK1和NF-κB信号决定CD8⁺ T细胞的交叉启动。
Science. 2015 Oct 16;350(6258):328-34. doi: 10.1126/science.aad0395. Epub 2015 Sep 24.
3
RIP3 induces apoptosis independent of pronecrotic kinase activity.RIP3诱导细胞凋亡，与坏死前激酶活性无关。
Mol Cell. 2014 Nov 20;56(4):481-95. doi: 10.1016/j.molcel.2014.10.021.
4
Distinct roles of RIP1-RIP3 hetero- and RIP3-RIP3 homo-interaction in mediating necroptosis.RIP1-RIP3异源相互作用和RIP3-RIP3同源相互作用在介导坏死性凋亡中的不同作用。
Cell Death Differ. 2014 Nov;21(11):1709-20. doi: 10.1038/cdd.2014.77. Epub 2014 Jun 6.
5
Translocation of mixed lineage kinase domain-like protein to plasma membrane leads to necrotic cell death.混合谱系激酶结构域样蛋白易位至质膜导致坏死性细胞死亡。
Cell Res. 2014 Jan;24(1):105-21. doi: 10.1038/cr.2013.171. Epub 2013 Dec 24.
6
Mouse receptor interacting protein 3 does not contain a caspase-recruiting or a death domain but induces apoptosis and activates NF-kappaB.小鼠受体相互作用蛋白3不包含半胱天冬酶招募结构域或死亡结构域，但可诱导细胞凋亡并激活核因子κB。
Mol Cell Biol. 1999 Oct;19(10):6500-8. doi: 10.1128/MCB.19.10.6500.
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Autoproteolytic activation of pro-caspases by oligomerization.前半胱天冬酶通过寡聚化进行自身蛋白水解激活。
Mol Cell. 1998 Jan;1(2):319-25. doi: 10.1016/s1097-2765(00)80032-5.
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