Accepted_test
The toll-like receptor (TLR) protein family plays a crucial role in the innate immune system of humans. The human body contains 10 distinct TLRs, labeled TLR1 through TLR10. When activated, these receptors trigger the innate immune response and inflammatory processes. Research has shown that TLRs contribute to varying extents in the development of infectious diseases, autoimmune disorders, and neurodegenerative conditions.
Structurally, TLRs are type 1 transmembrane proteins characterized by large extracellular and intracellular domains connected by a single alpha-helical transmembrane segment. These receptors carry out their functions as homo- or heterodimers. Despite extensive investigation into TLRs, many unresolved questions remain regarding the structural arrangements of their intracellular domains and the mechanisms by which they become activated to initiate transduction of the immune response signaling.
Using the TIR (Toll/IL-1 Receptor) domain of TLR1 as a representative example, this study investigated the dynamics and spatial structures of this domain both in solution and crystalline states. The research demonstrated that the intracellular domains of TLRs possess metal-binding capabilities, specifically obtaining data showing their ability to bind zinc ions with nanomolar dissociation constants. Through experiments with point mutants of the TIR domains from TLRs, key amino acid residues necessary for zinc ion binding were identified within the protein sequences examined. The results further illustrate a functional analysis of TLRs, revealing the role of zinc ion binding in TLR activation and highlighting the functional significance of the previously identified crucial amino acid residues.