HMGB1 SIGNALS THROUGH TOLL-LIKE RECEPTOR (TLR) 4 AND TLR2
By Man Yu, Haichao Wang, A. Ding, D. Golenbock, E. Latz, C. Czura, M. Fenton, Kevin J. Tracey, Huan Yang. Shock, 2006
874 citations recorded by the source corpus.
Subfields: Clinical Biochemistry, Experimental and Cognitive Psychology, Immunology
View Paper: https://www.semanticscholar.org/paper/3cf18d8d6304e1be1aaca41856a772ad5c76bcb1
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In Clinical Biochemistry
In Immunology
Citations in the corpus
- Sterile inflammation: sensing and reacting to damage (2010, background): “Although several of the purified endogenous molecules, including HSPs, HMGB1 and uric acid, can induce the production of pro-inflammatory cytokines through TLR2 and/or TLR4 in vitro”
- Autophagy, ferroptosis, pyroptosis, and necroptosis in tumor immunotherapy (2022, background): “through TLR2 and TLR4 receptors activating transcription factors NF-κB and AP-1, triggering inflammation and cytokines’ production such as IL-6, TNFα, IL-8 needed for CD8+ T cells activation.(226) Through HMGB1 signaling, chemotherapy and radiotherapy-induced cell death leads to an increase in antig”
- A critical cysteine is required for HMGB1 binding to Toll-like receptor 4 and activation of macrophage cytokine release (2010, methodology): “To circumvent potential issues of bacterial contaminants or impurities attributable to recombinant bacterialderived proteins, here we constructed amammalian tumor cell line (CHO) that continuously secretes HMGB1 (10) (Fig.”