@article{6de75168647f4035b0b14ab4371abc54,
title = "O-GlcNAc Transferase Suppresses Inflammation and Necroptosis by Targeting Receptor-Interacting Serine/Threonine-Protein Kinase 3",
abstract = "The role of individual glucose metabolic pathways in innate immunity remains largely unknown. Li et al. demonstrate that attenuated O-linked β-N-acetylglucosamine (O-GlcNAc) signaling enhances TLR-induced innate immune response and necroptosis. Mechanistically, O-GlcNAcylation of the kinase RIPK3 blocks RHIM-domain-mediated protein interaction and downstream signaling activation.",
keywords = "HBP, O-GlcNAc, OGT, RIPK3, inflammation, necroptosis",
author = "Xinghui Li and Wei Gong and Hao Wang and Tianliang Li and Attri, {Kuldeep S.} and Lewis, {Robert E.} and Kalil, {Andre C.} and Fatema Bhinderwala and Robert Powers and Guowei Yin and Herring, {Laura E.} and Asara, {John M.} and Lei, {Yu L.} and Xiaoyong Yang and Rodriguez, {Diego A.} and Mao Yang and Green, {Douglas R.} and Singh, {Pankaj K.} and Haitao Wen",
note = "Funding Information: We thank A.S. Baldwin for the NF-κB-driven luciferase reporter construct and the expression plasmids for IKK1, IKK2, and RELA; F.K. Chan for the RIPK3 WT and mutant expression plasmids; H.K. Lin for the TRAF6 expression plasmid; X. Yu for the OGT expression plasmid; E.S. Mocarski for Ripk3K51A bone marrow cells; V.M. Dixit for Ripk3−/− mice; J.M. Murphy for Mlkl−/− mice; and M. Yuan for the metabolomics assay. This work was supported by National Institutes of Health (NIH) grants R01GM120496 to H.W.; 5P01CA120964 and 5P30CA006516 to J.M.A.; P30CA016086 to the UNC Lineberger Comprehensive Cancer Center; R01CA163649, R01CA210439, and R01CA216853 to P.K.S.; P30GM103335 and P20GM113126 to R.P.; R00DE024173 and R01DE026728 to Y.L.L.; R01DK102648 to X.Y.; and R37AI044828 and R35CA231620 to D.R.G. Metabolic tracer experiments were performed in facilities renovated under NIH grant RR015468-01. Funding Information: We thank A.S. Baldwin for the NF-κB-driven luciferase reporter construct and the expression plasmids for IKK1, IKK2, and RELA; F.K. Chan for the RIPK3 WT and mutant expression plasmids; H.K. Lin for the TRAF6 expression plasmid; X. Yu for the OGT expression plasmid; E.S. Mocarski for Ripk3 K51A bone marrow cells; V.M. Dixit for Ripk3 −/− mice; J.M. Murphy for Mlkl −/− mice; and M. Yuan for the metabolomics assay. This work was supported by National Institutes of Health (NIH) grants R01GM120496 to H.W.; 5P01CA120964 and 5P30CA006516 to J.M.A.; P30CA016086 to the UNC Lineberger Comprehensive Cancer Center; R01CA163649 , R01CA210439 , and R01CA216853 to P.K.S.; P30GM103335 and P20GM113126 to R.P.; R00DE024173 and R01DE026728 to Y.L.L.; R01DK102648 to X.Y.; and R37AI044828 and R35CA231620 to D.R.G. Metabolic tracer experiments were performed in facilities renovated under NIH grant RR015468-01 . Publisher Copyright: {\textcopyright} 2019 Elsevier Inc.",
year = "2019",
month = mar,
day = "19",
doi = "10.1016/j.immuni.2019.01.007",
language = "English (US)",
volume = "50",
pages = "576--590.e6",
journal = "Immunity",
issn = "1074-7613",
publisher = "Cell Press",
number = "3",
}