The DOI matches its Crossref record; 43 of the 43 references it cites were found in a registry or an index.
High mobility group box 1 protein interacts with multiple Toll-like receptors
Abstract
High mobility group box 1 (HMGB1), originally described as a DNA-binding protein, can also be released extracellularly and functions as a late mediator of inflammatory responses. Although recent reports have indicated that the receptor for advanced glycation end products (RAGE) as well as Toll-like receptor (TLR)2 and TLR4 are involved in cellular activation by HMGB1, there has been little evidence of direct association between HMGB1 and these receptors. To examine this issue, we used fluorescence resonance energy transfer (FRET) and immunoprecipitation to directly investigate cell surface interactions of HMGB1 with TLR2, TLR4, and RAGE. FRET images in RAW264.7 macrophages demonstrated association of HMGB1 with TLR2 and TLR4 but not RAGE. Transient transfections into human embryonic kidney-293 cells showed that HMGB1 induced cellular activation and NF-κB-dependent transcription through TLR2 or TLR4 but not RAGE. Coimmunoprecipitation also found interaction between HMGB1 and TLR2 as well as TLR4, but not with RAGE. These studies provide the first direct evidence that HMGB1 can interact with both TLR2 and TLR4 and also supply an explanation for the ability of HMGB1 to induce cellular activation and generate inflammatory responses that are similar to those initiated by LPS.
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Cites
Release of chromatin protein HMGB1 by necrotic cells triggers inflammation
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HMG-1 as a Late Mediator of Endotoxin Lethality in Mice
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Self-citationMD-2, a Molecule that Confers Lipopolysaccharide Responsiveness on Toll-like Receptor 4
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Toll-like Receptor-4 Mediates Lipopolysaccharide-induced Signal Transduction
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The Receptor for Advanced Glycation End Products (RAGE) Is a Cellular Binding Site for Amphoterin
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Reversing established sepsis with antagonists of endogenous high-mobility group box 1
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Cited by
Origin and physiological roles of inflammation
Medzhitov, R. (2008) · Nature · doi:10.1038/nature07201 · Cited by 6,618
Immunogenic cell death and DAMPs in cancer therapy
Krysko, D. V., Garg, A. D., Kaczmarek, A., Krysko, O., Agostinis, P., & Vandenabeele, P. (2012) · Nature Reviews Cancer · doi:10.1038/nrc3380 · Cited by 3,223
Apetoh, L., Ghiringhelli, F., Tesniere, A., Obeid, M., Ortiz, C., Criollo, A., Mignot, G., Maiuri, M. C., Ullrich, E., Saulnier, P., et al. (2007) · Nature Medicine · doi:10.1038/nm1622 · Cited by 3,056
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Metadata
- Authors
- Park, J. S., Gamboni-Robertson, F., He, Q., Svetkauskaite, D., Kim, J.-Y., Strassheim, D., Sohn, J.-W., Yamada, S., Maruyama, I., Banerjee, A., Ishizaka, A., & Abraham, E.
- Venue
- American Journal of Physiology-Cell Physiology
- Publisher
- American Physiological Society
- Published
- 2006-03
- Volume
- 290
- Issue
- 3
- Pages
- C917-C924
- ISSN
- 0363-6143 (ISSN-L)
- 1522-1563
- OpenAlex
- W2125175295
- Cited by
- 932
- References
- 43
- FWCI
- 25.61
- Type
- journal article
- Language
- en
- Open access
- closed
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