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NLRX1 并不抑制 MAVS 依赖性抗病毒信号转导。

NLRX1 does not inhibit MAVS-dependent antiviral signalling.

机构信息

Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, ON, Canada.

出版信息

Innate Immun. 2013;19(4):438-48. doi: 10.1177/1753425912467383. Epub 2012 Dec 4.

Abstract

NLRX1 is a member of the Nod-like receptor family of intracellular sensors of microbial- and danger-associated molecular patterns. NLRX1 has a N-terminal mitochondrial addressing sequence that localizes the protein to the mitochondrial matrix. Recently, conflicting reports have been presented with regard to the putative implication of NLRX1 as a negative regulator of MAVS-dependent cytosolic antiviral responses. Here, we generated a new NLRX1 knockout mouse strain and observed that bone marrow-derived macrophages and murine embryonic fibroblasts from NLRX1-deficient mice displayed normal antiviral and inflammatory responses following Sendai virus infection. Importantly, wild type and NLRX1-deficient mice exhibited unaltered antiviral and inflammatory gene expression following intranasal challenge with influenza A virus or i.p. injection of Poly (I:C). Together, our results demonstrate that NLRX1 does not participate in the negative regulation of MAVS-dependent antiviral responses.

摘要

NLRX1 是细胞内微生物和危险相关分子模式的 Nod 样受体家族的成员。NLRX1 具有 N 端线粒体定位序列,将蛋白定位到线粒体基质中。最近,有关 NLRX1 作为 MAVS 依赖性细胞抗病毒反应的负调节剂的假定作用,出现了相互矛盾的报告。在这里,我们生成了一种新的 NLRX1 敲除小鼠品系,并观察到骨髓来源的巨噬细胞和 NLRX1 缺陷型小鼠的胚胎成纤维细胞在感染仙台病毒后表现出正常的抗病毒和炎症反应。重要的是,野生型和 NLRX1 缺陷型小鼠在鼻内接种流感病毒或腹腔注射 Poly(I:C)后,抗病毒和炎症基因表达没有改变。总之,我们的结果表明 NLRX1 不参与 MAVS 依赖性抗病毒反应的负调节。

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