Description
Product Characteristics: The monoclonal antibody GD2.F4 reacts with human TLR1. Toll-like receptors (TLR) are highly conserved throughout evolution and play an essential role in recognizing conserved motifs found in various pathogens and initiating an appropriate innate immune response. In human, ten members of the TLR family have been identified as type I transmembrane signaling receptors containing multiple copies of leucine rich repeats in the extracellular domain and an interleukin-1 (IL-1) receptor motif in the cytoplasmic domain. Mammalian responsiveness to microbial products may be mediated by combinations of TLRs, for example a co-operative effect is observed between TLR1 and TLR2 in response to bacterial lipoproteins. On the other hand, TLR 1 was shown to have the capacity to abrogate TLR4 signaling. In general, TLR1 is expressed at higher levels as compared to other TLRs. The highest expression of TLR1 is found in monocytes but it can also be expressed by macrophages, dendritic cells, B, T, and NK cells. In recent studies, several human TLR1 polymorphisms have been associated with impaired mycobacterial signaling and susceptibility to tuberculosis. Aliases CD281, toll-like receptor 1 Immunogen TLR1Fc
Target Information: The protein encoded by this gene is a member of the Toll-like receptor (TLR) family which plays a fundamental role in pathogen recognition and activation of innate immunity. TLRs are highly conserved from Drosophila to humans and share structural and functional similarities. They recognize pathogen-associated molecular patterns (PAMPs) that are expressed on infectious agents, and mediate the production of cytokines necessary for the development of effective immunity. The various TLRs exhibit different patterns of expression. This gene is ubiquitously expressed, and at higher levels than other TLR genes. Different length transcripts presumably resulting from use of alternative polyadenylation site, and/or from alternative splicing, have been noted for this gene. [provided by RefSeq, Jul 2008]