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• W2766093054 abstract "In this chapter we treat ubiquitinylation and how it leads to the activation of the NFKB and IRF3 pathways. The context is innate immunity, and we start by describing pathogen-associated molecular patterns receptors, among which the Toll-like receptors (TLR), on the dendritic cell. We focus on TLR4 and its ligand, lipopolysaccharide (LPS), a cell-wall component of Gram-negative bacteria. After a brief overview of the NFKB and ankyrin protein family, we describe the signaling complexes that assemble around dimerized TLR4, a process in which death domains and K63-ubiquitin chains play essential roles. Recruitment of protein kinases (IKBKB, CHUK, MAP3K7, and TKB1) causes activation of NFKB/RELA and IRF3. A set of MAP kinases is also activated of which MAPK8 (JNK1) phosphorylates and activates JUN and ATF. We then show how JUN/ATF, NFKB/RELA, and IRF3 take part in a transcriptional complex, the “enhanceosome,” which directs transcription of genes encoding inflammatory mediators. The last section of the chapter discusses the ubiquitin process, the different E3-ubiquitin ligases, and the different types of ubiquitin chains." @default.
• W2766093054 created "2017-11-10" @default.
• W2766093054 creator A5007964369 @default.
• W2766093054 date "2016-01-01" @default.
• W2766093054 modified "2023-10-16" @default.
• W2766093054 title "Activation of the Innate Immune System" @default.
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• W2766093054 doi "https://doi.org/10.1016/b978-0-12-394803-8.00013-9" @default.
• W2766093054 hasPublicationYear "2016" @default.
• W2766093054 type Work @default.

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