Abstract：
Among teleost NLRs, NLR-C subfamily is a large group of proteins that were teleost-specific and evolution analysis showed that NLR-Cs are most likely to evolve from NLRC3 gene (thus also called as NLRC3Ls). Presently, although there have been rich studies investigating teleost NLRC3 and NLRC3L, the data on the regulatory mechanism was limited. In this study, immune regulation of inflammatory signaling pathway mediated by common carp NLRC3L gene (CcNLRC) has been investigated. Confocal microscopy analysis showed that CcNLRC was located in cytoplasm, and in HEK293T cells, dual-luciferase reporter assay showed the regulation of NF-κB signaling by CcNLRC, in which CcNLRC could alter/decrease RIPK2-induced activation of NF-κB. These results indicated that CcNLRC may function as a negative NLR in the regulation of inflammatory response in common carp. Our data will allow to gain more insights into the molecular mechanism of teleost specific NLR (NLRC3L).
摘要：
在teleostNLR中，NLR-C亚家族是一组具有硬骨特异性的蛋白质，进化分析表明NLR-C最有可能从NLRC3基因（因此也称为NLRC3L）进化而来。目前,尽管已经有丰富的研究调查硬骨鱼NLRC3和NLRC3L，有关监管机制的数据有限。在这项研究中,本文对鲤鱼NLRC3L基因(CcNLRC)介导的炎症信号通路的免疫调节进行了研究。共聚焦显微镜分析表明，CcNLRC位于细胞质中，在HEK293T细胞中，双荧光素酶报告基因实验显示CcNLRC对NF-κB信号的调节，其中CcNLRC可以改变/降低RIPK2诱导的NF-κB活化。这些结果表明，CcNLRC可能在调节鲤鱼的炎症反应中起负NLR的作用。我们的数据将使人们对硬骨鱼特异性NLR（NLRC3L）的分子机制有更多的了解。
