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• W2219188266 endingPage "13" @default.
• W2219188266 startingPage "1" @default.
• W2219188266 abstract "Viral infection activates danger signals that are transmitted via the retinoic acid-inducible gene 1-like receptor (RLR), nucleotide-binding oligomerization domain-like receptor (NLR), and Toll-like receptor (TLR) protein signaling cascades. This places host cells in an antiviral posture by up-regulating antiviral cytokines including type-I interferon (IFN-I). Ubiquitin modifications and cross-talk between proteins within these signaling cascades potentiate IFN-I expression, and inversely, a growing number of viruses are found to weaponize the ubiquitin modification system to suppress IFN-I. Here we review how host- and virus-directed ubiquitin modification of proteins in the RLR, NLR, and TLR antiviral signaling cascades modulate IFN-I expression." @default.
• W2219188266 created "2016-06-24" @default.
• W2219188266 creator A5019562426 @default.
• W2219188266 creator A5051823046 @default.
• W2219188266 creator A5084210146 @default.
• W2219188266 date "2015-12-28" @default.
• W2219188266 modified "2023-10-14" @default.
• W2219188266 title "Ubiquitin in the activation and attenuation of innate antiviral immunity" @default.
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