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Product Name | TLR2/TLR1 ligand control |
Description | PHC-SKKKK is a synthetic lipopeptide (LP). Bacterial lipopeptides are strong modulators that activate early host responses after infection as well as initiating adjuvant effects on the adaptive immune system. Signaling of lipopeptides occurs in cells via Toll-like receptor 2 (TLR2)-TLR1 or TLR2-TLR6 heteromers. TLRs are important pattern-recognition receptors (PRR) which are evolutionary-conserved and recognize invading pathogens via pathogen-associated molecular patterns (PAMP). Receptor expression is cell type dependent and the activation of inflammatory target genes is ligand specific, creating unique cellular responses. LP, a component from the bacterial cell membrane, has a strong immunostimulatory effect and is an initiator of the primary innate reaction of e.g. macrophages and epithelial cells. Signaling through TLR2-TLRx heteromers by LP leads to the formation of an active signaling complex that includes MyD88 and the IL-1R-associated kinase (IRAK) proteins, initiating NF-κB mediated cytokine production. The number of fatty acids couples to the N-terminus of the peptide determine the ligand preference for the specific TLR2 heteromers. Triacylated LP are recognized by THR2/1 heterodimers, while diacylated LP are recognized by TLR2/6 complexes. It has been demonstrated that both the lipid moiety as well as the whole molecular structure are involved in the specificity of the interaction of TLR2-TLR6 heteromers. Synthetic LP PHC-SKKKK is an appropriate control compound for the stimulation of TLR2 with lipopeptides. It has similar physicochemical properties as Pam3Cys-SKKKK. PHC-SKKKK cannot activate TLR2 and is therefore suitable as triacylated negative control. |
Size | 50 µg |
Concentration | Lyophilized product in tert-Butanol and water, containing 50 µg. |
Applications | n/a |
Other Names | PHC-Ser-(Lys)4 x 3 TFA |
Gene, Accession, CAS # | n/a |
Catalog # | HC4069 |
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Order / More Info | TLR2/TLR1 ligand control from HYCULT BIOTECH |
Product Specific References | n/a |
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