生物
信号转导
细胞生物学
蛋白酶体
NF-κB
先天免疫系统
信号转导衔接蛋白
泛素
Toll样受体
NFKB1型
αBκ
受体
癌症研究
转录因子
生物化学
基因
作者
Baolan Cao,Yan Zhao,Qiang Luo,Chen Ya,Tianjun Xu,Yuena Sun
标识
DOI:10.1016/j.fsi.2023.108683
摘要
Myeloid differentiation factor 88 (MyD88) is the canonical adaptor for inflammatory signaling pathways downstream from members of the Toll-like receptor (TLR) and interleukin-1 (IL-1) receptor families, which activates the NF-κB signaling pathway and regulates immune and inflammatory responses. In this study, we found that Vinculin B (Vclb) is an inhibitor in the NF-κB signaling pathway, and its inhibitory effect was enhanced by LPS induction. Furthermore, Vclb inhibits NF-κB activation by targeting MyD88, thereby suppressing the production of inflammatory cytokines. Mechanistically, Vclb inhibits the NF-κB signaling pathway by targeting MyD88 ubiquitin-proteasome pathway. In summary, our study reveals that Vclb inhibits NF-κB signaling activation and mediates innate immunity in teleosts via the ubiquitin-proteasome pathway of MyD88.
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