TLR3型
MAPK/ERK通路
干扰素
基因表达
生物
信号转导
分子生物学
蛋白激酶R
基因
细胞生物学
基因表达调控
激酶
病毒学
Toll样受体
蛋白激酶A
受体
先天免疫系统
丝裂原活化蛋白激酶激酶
遗传学
作者
Shawn Freed,Danielle S. Baldi,Jason A. Snow,Sierra R. Athen,Zachary Guinn,T. Scott Pinkerton,Thomas M. Petro,Tyler C. Moore
出处
期刊:FEBS Letters
[Wiley]
日期:2021-10-11
卷期号:595 (21): 2665-2674
被引量:6
标识
DOI:10.1002/1873-3468.14200
摘要
Toll‐like receptor 3 (TLR3) recognizes viral double‐stranded RNA (or the synthetic dsRNA analog poly I:C) and induces a signal transduction pathway that results in activation of transcription factors that induce expression of antiviral genes including type I interferon (IFN‐I). Secreted IFN‐I positively feeds back to amplify antiviral gene expression. In this report, we study the role of MEK/ERK MAP kinase in modulating antiviral gene expression downstream of TLR3. We find MEK/ERK is a negative regulator of antiviral gene expression by limiting expression of IFN‐β. However, MEK/ERK does not limit antiviral responses downstream of the type I interferon receptor. These findings provide insights into regulatory mechanisms of antiviral gene expression and reveal potential targets for modulating antiviral immunity.
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