A cell-permeable, water-soluble synthetic cationic lipohexapeptide analog of the immunologically active N-terminal portion of bacterial lipoprotein that potently activates monocytes and macrophages. Induces the release of IL-1, IL-6, TNF-α, superoxide, and NO. Promotes the translocation of NF-κB, enhances tyrosine protein phosphorylation and activation of ERK1/2 and MEK1/2. Acts as a selective agonist of TLR2 (Toll-like receptor 2).
A cell-permeable, water-soluble, synthetic, cationic lipohexapeptide analog of the immunologically active N-terminal portion of bacterial lipoprotein that potently activates monocytes and macrophages. Induces the release of IL-1, IL-6, TNF-α, superoxide and NO. Promotes the translocation of NF-κB, enhances tyrosine protein phosphorylation, and activates ERK1/2 and MEK1/2. Acts as a selective TLR-2 (Toll-like receptor 2) agonist.
pam3csk4 is an agonist of toll-like receptor 1/2 (tlr1/2) [1].toll-like receptors (tlrs) are proteins that play an important role in the innate immune system. tlrs are mainly expressed in sentinel cells that recognize molecules derived from microbes and then activate immune cell responses.pam3csk4 is a tlr1/2 agonist. pam3csk4 increased tyrosine phosphorylation of plcγ2 and the adaptor protein lat in a syk- and src-dependent way. also, pam3csk4 evoked platelet activation [1].in a mouse rhinitis model sensitized to dermatophagoides farinae allergen, pam3csk4 significantly improved the nasal allergic symptoms and reduced total inflammation cells and the eosinophils in bronchoalveolar lavage fluid (balf). also, pam3csk4 significantly increased ifn-γ release and decreased the levels of il-13 and total ige [2]. pam3csk4 induced the production of both no and tnf-ɑ by macrophages [3]. in a murine asthma model challenged with ova, pam3csk4 significantly reduced eosinophilia and total inflammatory cell infiltrate in balf and inhibited the secretion of il-4 and il-5 induced by ova. also, pam3csk4 reduced the level of ige and increased the production of il-12 [4].
