猪流行性腹泻病毒
生物
维罗细胞
病毒学
病毒复制
基因敲除
先天免疫系统
干扰素
信号转导
病毒
细胞生物学
基因
免疫系统
遗传学
作者
Sujie Dong,Ning Kong,Huiyong Shen,Youwen Li,Wenzhen Qin,Huanjie Zhai,Xueying Zhai,Xinyu Yang,Chenqian Ye,Manqing Ye,Changlong Liu,Lingxue Yu,Zhixin Hao,Tong Wu,Hai Yu,Wen Zhang,Guangzhi Tong,Tongling Shan
标识
DOI:10.1016/j.vetmic.2022.109577
摘要
KLF16, a member of KLFs (Krüppel-like factors), contributes to the progression of a variety of cancer types. There is, however, still uncertain regarding the role of KLF16 in viral replication and the signaling mechanism of type I IFN. It was discovered that KLF16 inhibited the replication of porcine epidemic diarrhea virus (PEDV) through the type I IFN signaling pathway. Besides, it can also be found that the expression of KLF16 was down-regulated after PEDV infection of LLC-PK1 cells. Furthermore, overexpression of KLF16 inhibited the replication of PEDV in Vero cells as well as LLC-PK1 cells, whereas the replication of PEDV was promoted by the knockdown of KLF16. KLF16 up-regulated the expression of interferons (IFNs) via the TRAF6-pTBK1-pIRF3 pathway with the aim of promoting the host antiviral innate immune response. In addition, the obtained findings proved that KLF16 plays a novel role in antiviral action, thereby offering novel possibilities for preventing and controlling PEDV.
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