2. Signaling Pathways
  3. Immunology/Inflammation
  4. Toll-like Receptor (TLR)
  5. TLR6 Isoform

TLR6

TLR6 functions as a cell-surface pattern-recognition receptor by forming the TLR2/6 heterodimer, which recognizes di-acylated lipopeptide signals and initiates innate immune activation[1]. Mechanistically, TLR2/6 signaling activates NF-κB-dependent inflammatory pathways, leading to cytokine outputs such as IL-6, IL-1β, and TNF-α in experimental cell models[2]. In disease models, TLR6 variants were identified in Kawasaki disease susceptibility, and TLR6 rs56245262 genotype was associated with differential IL-6 expression and higher erythrocyte sedimentation rate[3]. Compared with TLR1/2, TLR2/6 shows heterodimer-specific biology: Pam2CSK4, but not Pam3CSK4, accelerated leukemia and death in an NHD13 mouse model of myelodysplastic syndrome[4]. For experimental applications, FSL-1 and Pam2CSK4 serve as TLR2/6 agonists, while sensitive NF-κB reporter platforms detect TLR2/6 ligands at low concentrations for ligand characterization[5].

TLR6 Related Products (3):

Cat. No. Product Name Effect Purity
  • HY-P2036A
    FSL-1 TFA
    		Agonist 99.81%
    FSL-1 TFA, a bacterial-derived toll-like receptor 2/6 (TLR2/6) agonist, enhances resistance to experimental HSV-2 infection. FSL-1 TFA induces MMP-9 production through TLR2 and NF-κB/AP-1 signaling pathways in monocytic THP-1 cells.
  • HY-P2036
    FSL-1
    		Agonist 99.22%
    FSL-1, a bacterial-derived toll-like receptor 2/6 (TLR2/6) agonist, enhances resistance to experimental HSV-2 infection.
  • HY-P10586
    Macrophage-activating lipopeptide 2
    		Activator
    Macrophage-activating lipopeptide 2 (MALP-2) is an agonist of Toll like receptors TLR-2/TLR-6. Macrophage-activating lipopeptide-2 can enhance endothelial nitric oxide synthase (eNOS) phosphorylation and endothelial cell release of NO, thereby improving vasodilation. Macrophage-activating lipopeptide-2 can enhance endothelial adhesion of white blood cells and improve perfusion recovery and collateral growth in the hind limbs of hypercholesterolemic Apoe deficient mice undergoing experimental femoral artery ligation (FAL).