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• W3001799229 endingPage "713.e4" @default.
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• W3001799229 abstract "Receptor-interacting protein kinase 1 (RIPK1) and 3 (RIPK3) are well known for their capacity to drive necroptosis via mixed-lineage kinase-like domain (MLKL). Recently, RIPK1/3 kinase activity has been shown to drive inflammation via activation of MAPK signaling. However, the regulatory mechanisms underlying this kinase-dependent cytokine production remain poorly understood. In the present study, we establish that the kinase activity of RIPK1/3 regulates cytokine translation in mouse and human macrophages. Furthermore, we show that this inflammatory response is downregulated by type I interferon (IFN) signaling, independent of type I IFN-promoted cell death. Specifically, low-level constitutive IFN signaling attenuates RIPK-driven activation of cap-dependent translation initiation pathway components AKT, mTORC1, 4E-BP and eIF4E, while promoting RIPK-dependent cell death. Altogether, these data characterize constitutive IFN signaling as a regulator of RIPK-dependent inflammation and establish cap-dependent translation as a crucial checkpoint in the regulation of cytokine production." @default.
• W3001799229 created "2020-01-30" @default.
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• W3001799229 date "2020-01-01" @default.
• W3001799229 modified "2023-10-15" @default.
• W3001799229 title "Constitutive Interferon Attenuates RIPK1/3-Mediated Cytokine Translation" @default.
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• W3001799229 doi "https://doi.org/10.1016/j.celrep.2019.12.073" @default.
• W3001799229 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/7183097" @default.
• W3001799229 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/31968247" @default.
• W3001799229 hasPublicationYear "2020" @default.
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• W3001799229 citedByCount "21" @default.

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