The structural basis of lipopolysaccharide recognition by the TLR4–MD-2 complex
By B. Park, D. Song, Ho Min Kim, Byong-Seok Choi, Hayyoung Lee, Jie-Oh Lee. Nature, 2009
2,359 citations recorded by the source corpus.
Subfields: Epidemiology, Immunology, Microbiology
View Paper: https://www.semanticscholar.org/paper/e382296945d48d836ff49fb156a6c0355c435459
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In Epidemiology
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In Microbiology
Citations in the corpus
- A Comparative Review of Toll-Like Receptor 4 Expression and Functionality in Different Animal Species (2014, background): “Binding of LPS also requires the MD-2 protein, which associates with the extracellular domain of TLR4 (34).”
- Hyaluronan as an Immune Regulator in Human Diseases (2011, neutral): “However, MD-2 is usually associated with lipid recognition and binding (211, 336, 343).”
- The Structural Biology of Toll-Like Receptors (2011, background): “The TLR-ECDs also contain structures that cap the N and C-terminal ends known as the LRR-NT and LRR-CT motifs, respectively (Figure 2).”
- Impact of Obesity and Metabolic Syndrome on Immunity. (2016, background): “In addition to these functions, HDL may alter inflammatory responses by neutralizing LPS—an immunostimulatory glycolipid located on the outer membrane of Gram-negative bacteria that activates innate immune responses via pattern recognition receptors (110, 111).”
- Pathogen Recognition by the Innate Immune System (2011, background): “Therefore, lipid A activates the TLR4 signaling pathway, but Eritoran does not [13, 14].”
- INFLAMMATION AND LIPID SIGNALING IN THE ETIOLOGY OF INSULIN RESISTANCE (2012, neutral): “Structural considerations (Park et al., 2009) and direct binding assays (Schaeffler et al., 2009) argue against the possibility that SFAs are direct ligands for Tlr4.”
- Initiation and perpetuation of NLRP3 inflammasome activation and assembly (2015, background): “If cardiolipin is a ligand for NLRP3 activation, it is possible that its recognition requires accessory proteins as is the case for TLR4/ MD2/Lipid A (160); therefore, determining other molecules that associate with the NLRP3 inflammasome complex is critical.”
- Pattern recognition receptors and inflammation. (2010, background): “The crystal structure of a complex comprising TLR4, MD2, and LPS revealed that two complexes of TLR4-MD2-LPS interact symmetrically to form a TLR4 homodimer (Park et al., 2009).”
- TLR4 and CD14 trafficking and its influence on LPS-induced pro-inflammatory signaling (2020, background): “A crystallographic analysis of the human TLR4/MD-2 complex with LPS bound has revealed that five of the six acyl chains of LPS are buried in the hydrophobic pocket of MD-2 while the sixth one interacts with TLR4 of another TLR4/MD-2 complex, and that the dimerization of the TLR4/MD-2 complexes is st”
- Insights into secondary metabolism from a global analysis of prokaryotic biosynthetic gene clusters. (2014, background): “…Institute of Biotechnology, Faculty of Life Sciences, University of Manchester, Manchester M1 7DN, UK 12Present address: Max Planck Institute for Marine Microbiology, Celsiusstraße 1, 28359 Bremen, Germany *Correspondence: fischbach@fischbachgroup.org http://dx.doi.org/10.1016/j.cell.2014.06.034”