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Merck Research Laboratories, Rahway, New Jersey
Correspondence: Dr. Patricia A. Detmers, Merck Research Laboratories, 126 East Lincoln Avenue, RY80W-250, Rahway, NJ 07065. E-mail: patricia_detmers{at}merck.com
Early events in the response of cells to lipopolysaccharide (LPS)
include activation of NF-
B and stress-activated MAP kinase
p38. Recent studies have shown that the human Toll-like receptor 2
(TLR2) mediates activation of NF-
B in response to commercial
preparations of LPS (comLPS), membrane lipoproteins, and Gram-positive
bacterial products. Here, we show that expression of TLR2 in human
embryonic kidney 293 cells enabled p38 phosphorylation in response to
comLPS, a synthetic bacterial lipoprotein, and B. subtilis.
Activation of p38 was confirmed by an in vitro kinase assay using ATF2
as substrate and by an assay measuring activation of the downstream
effector of p38, MAP kinase-activated protein kinase in cells. Thus,
TLR2 initiated the signaling pathway for p38 in response to
bacterial products.
Key Words: lipopolysaccharide signal transduction cell-surface molecules protein kinases infectious immunity bacteria
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