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- W2942276193 abstract "Stimulator of interferon genes (STING) is a key regulator of type I interferon and pro-inflammatory responses during infection, cellular stress, and cancer. Here, we reveal a mechanism for how STING balances activation of IRF3- and NF-κB-dependent transcription and discover that acquisition of discrete signaling modules in the vertebrate STING C-terminal tail (CTT) shapes downstream immunity. As a defining example, we identify a motif appended to the CTT of zebrafish STING that inverts the typical vertebrate signaling response and results in dramatic NF-κB activation and weak IRF3-interferon signaling. We determine a co-crystal structure that explains how this CTT sequence recruits TRAF6 as a new binding partner and demonstrate that the minimal motif is sufficient to reprogram human STING and immune activation in macrophage cells. Together, our results define the STING CTT as a linear signaling hub that can acquire modular motifs to readily adapt downstream immunity." @default.
- W2942276193 created "2019-05-03" @default.
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- W2942276193 date "2019-04-01" @default.
- W2942276193 modified "2023-10-18" @default.
- W2942276193 title "Modular Architecture of the STING C-Terminal Tail Allows Interferon and NF-κB Signaling Adaptation" @default.
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- W2942276193 doi "https://doi.org/10.1016/j.celrep.2019.03.098" @default.
- W2942276193 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/7733315" @default.
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