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Our results suggest that binding of microbial ligands to TLRs is one of the mechanisms that mediate interactions between coinfected microbes and HIV-1 in human tissues.
Binding of microbial ligands to these receptors leads to the induction of a variety of cellular factors that alter intracellular and extracellular environment and interfere directly or indirectly with the life cycle of the triggering pathogen.
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In the absence of microbial ligands and cell debris, binding of SP-D to macrophages by the CRD region was suggested to be anti-inflammatory by blocking p38 mitogen-activated protein kinases (p38 MAPK) [ 47].
Removal of microbial ligands (germ-free) alleviated these phenotypes in the mutants.
Mayer, A.K. et al. Differential recognition of TLR-dependent microbial ligands in human bronchial epithelial cells.
The identity of naturally occurring TLR9 microbial ligands has not yet been definitively established.
It has been demonstrated that the binding of different ligands to ERalpha results in the formation of unique ERalpha-ligand conformations.
Nevertheless, the ability of different cell types to recognize and respond to microbial ligands differs.
TLR2 recognizes multiple, structurally disparate microbial ligands, consistent with a requirement for co-receptors in ligand binding.
The Bet v1 fold: an ancient, versatile scaffold for binding of large, hydrophobic ligands.
Davies, D. R. et al. Unique motifs and hydrophobic interactions shape the binding of modified DNA ligands to protein targets.
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