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The E3 Ubiquitin Ligase AMFR and INSIG1 Bridge the Activation of TBK1 Kinase by Modifying the Adaptor STING

Wang, Qiang, Liu, Xing, Cui, Ye, Tang, Yijun, Chen, Wei, Li, Senlin, Yu, Huansha, Pan, Youdong, Wang, Chen·2014·Immunity
DOI 10.1016/j.immuni.2014.11.011
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Abstract

Stimulator of interferon genes (STING, also known as MITA, ERIS, or MPYS) is essential for host immune responses triggered by microbial DNAs. However, the regulatory mechanisms underlying STING-mediated signaling are not fully understood. We report here that, upon cytoplasmic DNA stimulation, the endoplasmic reticulum (ER) protein AMFR was recruited to and interacted with STING in an insulin-induced gene 1 (INSIG1)-dependent manner. AMFR and INSIG1, an E3 ubiquitin ligase complex, then catalyzed the K27-linked polyubiquitination of STING. This modification served as an anchoring platform for recruiting TANK-binding kinase 1 (TBK1) and facilitating its translocation to the perinuclear microsomes. Depletion of AMFR or INSIG1 impaired STING-mediated antiviral gene induction. Consistently, myeloid-cell-specific Insig1(-/-) mice were more susceptible to herpes simplex virus 1 (HSV-1) infection than wild-type mice. This study uncovers an essential role of the ER proteins AMFR and INSIG1 in innate immunity, revealing an important missing link in the STING signaling pathway.

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  • INSIG1 is essential for STING pathway-mediated antiviral immunity and suppresses NLRP3 inflammasome activation and IL-1β production.

    “INSIG1 is essential for the stimulator of interferon genes (STING) pathway-mediated antiviral immunity and suppresses the NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome activation and IL-1β production31,32.”

    From Macrophage INSIG1 deficiency drives psoriasiform dermatitis via the SREBP2-STAT1 axis (2026) · cites this paper as [31]

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Cited by

Sorted by citations

Metadata

Authors
Wang, Q., Liu, X., Cui, Y., Tang, Y., Chen, W., Li, S., Yu, H., Pan, Y., & Wang, C.
Venue
Immunity
Publisher
Elsevier BV
Published
2014-12
Volume
41
Issue
6
Pages
919-933
ISSN
1074-7613
DOI
10.1016/j.immuni.2014.11.011
Cited by
358
References
4
Language
en
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