adaptor protein

(redirected from Adaptor molecules)

adaptor protein

[ə′dap·tər ‚prō‚tēn]
(cell and molecular biology)
A specialized protein that links protein components of the signaling pathway, thereby aiding intracellular signal transduction.
References in periodicals archive ?
Once TLR4 recognize the PAMPs, it triggers the recruitment of adaptor molecules (MAL) and initiates downstream signaling which leads to the activation of nuclear factor kappa B (NF-[kappa]B).
The stimulation of TLRs by the respective ligands results in the recruitment of downstream adaptor molecules, such as myeloid differentiation factor 88 (MyD88), myeloid Toll/interleukin- (IL-) 1 receptor- (TIR-) domain-containing adaptor-inducing interferon-[beta] (TRIF a.ka.
These pathways are characterised depending on which of the adaptor molecules MyD88 or TRIF are involved.
It impairs TLR-4's ability to associate with adaptor molecules, namely, TIRAP (MyD88 pathway) and TRAM (TIR-domain-containing adapter-inducing interferon-[beta]-related adaptor molecule) (non-MyD88 pathway), blocking subsequent signal transduction.
Ii, "TAK-242 (resatorvid), a small-molecule inhibitor of Toll-like receptor (TLR) 4 signaling, binds selectively to TLR4 and interferes with interactions between TLR4 and its adaptor molecules," Molecular Pharmacology, vol.
Brenner, "Toll-like receptors and adaptor molecules in liver disease: update," Hepatology, vol.
Since MyD88 is a common adaptor molecule that mediates downstream signaling from all bacterial responsive TLRs, we hypothesized that MyD88 is required for the transient postnatal increase in liver Treg frequency.
They discuss innate antiviral responses in invertebrates and Toll-like receptors (TLR) in vertebrates, as well as the phylogenetic relationship of pathogen sensing, the downstream adaptor molecules, and the functional consequences; nucleic acid sensing pathways, alternative regulator mechanisms of TLR signaling RIG-I-like receptors, the contribution of LGP2 to antiviral immunity, mitochondrial immune signaling complex and DNA sensors, and the complexities of downstream signaling, the adaptor molecules involved, and the regulatory pathways; and the molecular mechanisms by which pathogens such as poxviruses, HIV, and influenza evade host innate immune mechanisms, the viral virulence factors responsible, and their interactions with the innate immune sensors.
TLR4 protein is activated by the binding of ligand (s) which leads to the recruitment of adaptor molecules, including myeloid differentiation protein 88 (MyD88) (Akira and Takeda 2004).
Investigation of Adaptor Molecules' Interactions with Toll-like Receptors (TLR) of the Mammalian Cornea: Roles of TRIF and MyD88 in TLR3 Expression and Mediated-Immune Response.
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