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- W1652312395 abstract "Abstract Upon contact with airway epithelial cells, bacterial products activate Ca2+ fluxes that are required for induction of NF-κB-dependent gene expression. TLR2 is apically displayed on airway cells, making it a likely transducer linking bacterial stimuli and kinases that affect Ca2+ release. Using biochemical and genetic approaches, we demonstrate that TLR2 ligands stimulate release of Ca2+ from intracellular stores by activating TLR2 phosphorylation by c-Src, and recruiting PI3K and phospholipase Cγ to affect Ca2+ release through inositol (1,4,5) trisphosphate receptors. In the absence of TLR2, murine macrophages as well as airway cells do not generate Ca2+ fluxes or induce proinflammatory signaling. Thus, Ca2+ participates as a second messenger in TLR2-dependent signaling and provides another target to modulate proinflammatory responses to bacterial infection." @default.
- W1652312395 created "2016-06-24" @default.
- W1652312395 creator A5053191381 @default.
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- W1652312395 date "2006-07-15" @default.
- W1652312395 modified "2023-09-29" @default.
- W1652312395 title "Activation of Ca2+-Dependent Signaling by TLR2" @default.
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- W1652312395 doi "https://doi.org/10.4049/jimmunol.177.2.1330" @default.
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