Anti-TLR6 (human), clone ABM1B50

TLR6 (Toll-like Receptor 6) is a member of the TLR (Toll-like receptor) family that plays a fundamental role in pathogen recognition and activation of innate immunity. TLR6 in complex with TLR2 specifically recognizes diacylated and, to a lesser extent, triacylated lipopeptides from Gram-positive bacteria and fungi. The activation cluster TLR2:TLR6:CD14:CD36 signals via MYD88 and TRAF6, leading to NF-kappaB activation, cytokine secretion and the inflammatory response. In complex with TLR2 recognizes MALP-2, STF, PSM and OspA-L, as well. In response to oxidized low-density lipoprotein (oxLDL) or amyloid-beta 42, TLR6 forms a heterodimer with TLR4. This complex rapidly internalizes and triggers inflammatory responses through the NF-kappaB-dependent MYD88 signaling or via TICAM1 signaling pathways. The complex promotes sterile inflammation in monocytes/macrophages. TLR6 has emerged as the most potent activator for ZNPs (Zinc Oxide Nanoparticles)-induced inflammatory responses. Various polymorphism have been associated with inflammatory and tumor pathologies. Protein function: Participates in the innate immune response to Gram- positive bacteria and fungi. Specifically recognizes diacylated and, to a lesser extent, triacylated lipopeptides (PubMed:20037584). In response to diacylated lipopeptides, forms the activation cluster TLR2:TLR6:CD14:CD36, this cluster triggers signaling from the cell surface and subsequently is targeted to the Golgi in a lipid-raft dependent pathway (PubMed:16880211). Acts via MYD88 and TRAF6, leading to NF-kappa-B activation, cytokine secretion and the inflammatory response. Recognizes mycoplasmal macrophage-activating lipopeptide-2kD (MALP-2), soluble tuberculosis factor (STF), phenol-soluble modulin (PSM) and B.burgdorferi outer surface protein A lipoprotein (OspA-L) cooperatively with TLR2 (PubMed:11441107). In complex with TLR4, promotes sterile inflammation in monocytes/macrophages in response to oxidized low-density lipoprotein (oxLDL) or amyloid-beta 42. In this context, the initial signal is provided by oxLDL- or amyloid- beta 42-binding to CD36. This event induces the formation of a heterodimer of TLR4 and TLR6, which is rapidly internalized and triggers inflammatory response, leading to the NF-kappa-B- dependent production of CXCL1, CXCL2 and CCL9 cytokines, via MYD88 signaling pathway, and CCL5 cytokine, via TICAM1 signaling pathway, as well as IL1B secretion (PubMed:11441107, PubMed:20037584). [The UniProt Consortium]