Abstract MyD88, IRAK4 and IRAK2 are critical signalling mediators of the TLR/IL1-R
superfamily. Here we report the crystal structure of the MyD88–IRAK4–IRAK2 death domain …

Abstract Mammalian Toll-like receptors (TLRs) recognize conserved products of microbial
metabolism and activate NF-κB and other signaling pathways through the adapter protein …

Signal transduction through Toll-like receptors (TLRs) originates from their intracellular
Toll/interleukin-1 receptor (TIR) domain, which binds to MyD88, a common adaptor protein …

The recognition of microbial pathogens by the innate immune system involves Toll-like
receptors (TLRs), which recognize pathogen-associated molecular patterns,,,,,,,,. Different …

Summary trans-autophosphorylation is among the most prevalent means of protein kinase
activation, yet its molecular basis is poorly defined. In Toll-like receptor and interleukin-1 …

Signal transduction by Toll-like receptor 2 (TLR2) and TLR4 requires the adaptors MyD88
and Mal (MyD88 adaptor-like) and serine/threonine kinases, interleukin-1 receptor …

Toll-like receptors (TLRs) are pivotal in triggering the innate immune response to pathogen
infection. Ligand binding induces receptor dimerization which facilitates the recruitment of …

Toll-like receptors (TLRs) mediate responses to pathogen-associated molecules as part of
the vertebrate innate immune response to infection. Receptor dimerization is coupled to …

The activation of Toll-like receptors (TLRs) is central to innate and adaptive immunity,,. All
TLRs use the adaptor MyD88 for signalling, but the mechanisms underlying the MyD88 …

Toll-like receptor (TLR) signaling is a key innate immunity response to pathogens.
Recruitment of signaling adapters such as MAL (TIRAP) and MyD88 to the TLRs requires …