...
首页> 外文期刊>The FEBS journal >Recognizing limits of Z-nucleic acid binding protein (ZBP1/DAI/DLM1) function
【24h】

Recognizing limits of Z-nucleic acid binding protein (ZBP1/DAI/DLM1) function

机译:识别Z-核酸结合蛋白的限制(ZBP1 / DAI / DLM1)功能

获取原文
获取原文并翻译 | 示例
           

摘要

Z-nucleic acid binding protein (ZBP)1 (also known as DAI and DLM1) is a pathogen sensor activated by double-strand character RNA to recruit receptor-interacting protein (RIP) kinase via a RIP homotypic interaction motif. The activation of receptor-interacting protein kinase (RIPK)3 and initiation of virus-induced necroptosis were initially reported in a landmark publication Uptonet al.(Cell Host Microbe11: 290, 2012) employing the DNA virus murine cytomegalovirus (MCMV). M45-encoded viral inhibitor of RIP activation prevents virus-induced necroptosis. Additional virus-encoded suppressors of necroptosis were then identified, including herpes simplex virus ICP6 and vaccinia virus E3L. Caspase-8 suppressors encoded by these DNA viruses block apoptosis, unleashing necroptosis mediated through Z-nucleic acid binding protein 1 (ZBP1) recruitment of RIPK3. These studies all utilized ZBP1-deficient mice generated by the Akira Lab (Zbp1(-/- AK)) to bring the significance of virus-induced necroptosis to light. C57BL/6 mice were chosen as controls based on the assumption that mutant mice were congenic; however, these mice were recently found to display an unexpected innate immune deficit, lacking C57BL/6-specific NK1.1 and Ly49H natural killer cell subpopulations important in the early control of MCMV infection. Short nucleotide polymorphism analysis ofZbp1(-/- AK) breeders revealed a mixed genetic background (similar to 71% C57BL/6 DNA and similar to 29% 129). Even though this level of 129 strain background does not alter ZBP1 cell-autonomous function as a sensor and mediator of necroptosis, it confounds innate immune response characteristics. In the future, genetic background must be carefully controlled before implicating ZBP1 function in response characteristics that shape immunity, inflammation, metabolism, and pathogenesis.
机译:Z-核酸结合蛋白(ZBP)1(也称为DAI和DLM1)是由双链RNA字符激活以招募受体相互作用蛋白(RIP)的病原体传感器激酶通过RIP同型相互作用基序。受体相互作用蛋白激酶(RIPK)3和病毒诱导的坏死的开始的激活最初报道的里程碑出版物Uptonet人(细胞宿主Microbe11:290,2012)。采用DNA病毒鼠巨细胞病毒(MCMV)。 M45-编码RIP活化防止病毒诱导性坏死的病毒抑制剂。那么性坏死的其它病毒编码的抑制进行鉴定,包括单纯疱疹病毒ICP6和痘苗病毒E3L。胱天蛋白酶-8抑制剂由这些DNA病毒块凋亡编码,释放出坏死的通过RIPK3的Z-核酸结合蛋白1(ZBP1)招募介导的。这些研究由晃实验室产生的所有使用ZBP1缺陷小鼠(ZBP1( - / - AK)),以使病毒诱导性坏死的重要意义,以光线。 C57BL / 6小鼠被选为基于的假设是突变小鼠同类系的控制;然而,这些小鼠最近发现显示意想不到的先天免疫赤字,缺乏C57BL / 6特定NK1.1和Ly49H自然杀伤细胞亚群在MCMV感染的早期控制是重要的。短核苷酸多态性分析ofZbp1( - / - AK)育种者揭示了混合的遗传背景(类似于71%C57BL / 6的DNA和相似〜29%129)。即使这种程度的129菌株背景不一样性坏死的一个传感器和介体的alter ZBP1细胞自主功能,它混淆先天免疫应答的特性。在未来,遗传背景,必须仔细响应特性牵连ZBP1函数形状免疫,炎症,代谢和发病之前进行控制。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号