TLRs (Toll-like receptors) are an important class of pathogen-sensing proteins, which signal the presence of a pathogen by activating transcription factors, such as NF-κB (nuclear factor κB). The TLR pathway to NF-κB activation involves multiple phosphorylation and ubiquitination events. Notably, TRAF-6 [TNF (tumour necrosis factor)-receptor-associated factor-6] Lys63 polyubiquitination is a critical step in the formation of signalling complexes, which turn on NF-κB. Here, the relative role of different IRAKs [IL-1 (interleukin 1)-receptor-associated kinases] in NF-κB activation is discussed. Further, I demonstrate how understanding one molecular mechanism whereby vaccinia virus inhibits NF-κB activation has led to a revealing of a key role for IRAK-2 in TRAF-6-mediated NF-κB activation.
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Conference Article| May 21 2008
Insights from vaccinia virus into Toll-like receptor signalling proteins and their regulation by ubiquitin: role of IRAK-2
Andrew G. Bowie
Andrew G. Bowie 1
1School of Biochemistry and Immunology, Trinity College Dublin, Dublin 2, Ireland
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Biochem Soc Trans (2008) 36 (3): 449–452.
January 16 2008
Andrew G. Bowie; Insights from vaccinia virus into Toll-like receptor signalling proteins and their regulation by ubiquitin: role of IRAK-2. Biochem Soc Trans 1 June 2008; 36 (3): 449–452. doi: https://doi.org/10.1042/BST0360449
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