A second binding site for double-stranded RNA in TLR3 and consequences for interferon activation
- 22 June 2008
- journal article
- research article
- Published by Springer Nature in Nature Structural & Molecular Biology
- Vol. 15 (7) , 761-763
- https://doi.org/10.1038/nsmb.1453
Abstract
We show that substrate specificity of Toll-like receptor 3 (TLR3) is due to the presence of two binding sites in the ectodomain, separated by 50 Å. This corresponds to two turns of a double-stranded RNA duplex, allowing differentiation between nucleic acids in the A- or B-type conformation. We propose that there are different arrangements of TLR3 ectodomains along the double-stranded RNA that could modulate the strength of the interferon response.Keywords
This publication has 21 references indexed in Scilit:
- Sequence- and target-independent angiogenesis suppression by siRNA via TLR3Nature, 2008
- The molecular structure of the TLR3 extracellular domainInnate Immunity, 2006
- The dsRNA binding site of human Toll-like receptor 3Proceedings of the National Academy of Sciences, 2006
- Induction of the interferon response by siRNA is cell type– and duplex length–dependentRNA, 2006
- The molecular structure of the Toll-like receptor 3 ligand-binding domainProceedings of the National Academy of Sciences, 2005
- Crystal Structure of Human Toll-Like Receptor 3 (TLR3) EctodomainScience, 2005
- Effects of Length and Location on the Cellular Response to Double-Stranded RNAMicrobiology and Molecular Biology Reviews, 2004
- Small Interfering RNAs Mediate Sequence-Independent Gene Suppression and Induce Immune Activation by Signaling through Toll-Like Receptor 3The Journal of Immunology, 2004
- Recognition of double-stranded RNA and activation of NF-κB by Toll-like receptor 3Nature, 2001
- Potent and specific genetic interference by double-stranded RNA in Caenorhabditis elegansNature, 1998