Authors
Xingmei Qi, Xue Zhu, Wenbiao Peng, Luoxue Hua, Xinru Xie, Chuncan Si, Meimei Lan, Zifan Zhuang, Siyi Ding, Ting Xu, Junjie Li, Yundi Zhang, Yifan Song, Yiping Yang, Yixue Cheng, Tao Guo, Linchao Li, Kezhen Wang
Published in
PLoS pathogens. Volume 22. Issue 10. Pages e1014701. Epub Oct 27, 2026.
Abstract
Innate immunity constitutes the body's first line of defense against pathogenic challenge, serving not only as a physical and cellular bulwark that rapidly curbs microbial proliferation but also as the essential rheostat that orchestrates downstream adaptive immune responses. Here, we identified MARK3, a serine/threonine protein kinase of the conserved MARK family, as a crucial regulator of innate antiviral immunity that promotes type I interferon (IFN-I) production in a kinase-dependent manner. Using both in vitro and in vivo models, we demonstrate that MARK3 exerts broad-spectrum antiviral activity via a signaling axis involving GEF-H1 and TBK1. Mechanistically, MARK3 directly interacts with GEF-H1 and phosphorylates it at Ser645. This phosphorylation event potentiates the activation of TBK1, leading to enhanced IRF3 phosphorylation. Activated IRF3 then translocates to the nucleus, where it triggers potent IFN-I induction and the downstream expression of interferon-stimulated genes (ISGs). Our study establishes MARK3 as an important antiviral kinase and defines the MARK3-GEF-H1-TBK1 axis as a novel signaling pathway driving interferon-mediated antiviral defense.
PMID:
42945342
Bibliographic data and abstract were imported from PubMed on 28 Oct 2026.
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