Members of the Toll-like receptor (TLR) family, named for the closely related Toll receptor in Drosophila, play a pivotal role in innate immune responses. TLRs recognize conserved motifs found in various pathogens and mediate defense responses. Triggering of the TLR pathway leads to the activation of NF-κB and subsequent regulation of immune and inflammatory genes. The TLRs and members of the IL-1 receptor family share a conserved stretch of approximately 200 amino acids known as the TIR domain. Upon activation, TLRs associate with a number of cytoplasmic adaptor proteins containing TIR domains including MyD88 (myeloid differentiation factor), MAL/TIRAP (MyD88-adaptor-like/TIR-associated protein), TRIF (Toll-receptor-associated activator of interferon), and TRAM (Toll-receptor-associated molecule). This association leads to the recruitment and activation of IRAK1 and IRAK4, which form a complex with TRAF6 to activate TAK1 and IKK. Activation of IKK leads to the degradation of IκB that normally maintains NF-κB inactivity by sequestering it in the cytoplasm.TLR3 functions as a receptor for double-stranded (ds)RNA typically associated with viral infection. It was originally shown to be specifically expressed in dendritic cells of the leukocyte family. TLR3 has also been found in placenta and lung, and can be induced by LPS in a variety of tissues. TLR3 is predominantly localized to early endosomes. Binding of dsRNA, or the analog polyinosine-polycytidylic acid (pIpC), to TLR3 triggers activation of transcription factors NF-κB and IRF3 through the adaptor protein TICAM-1/TRIF. TRIF associates with members of the TRAF family and with RIP that combine to activate NF-κB and IRF3.
Members of the Toll-like receptor (TLR) family, named for the closely related Toll receptor in Drosophila, play a pivotal role in innate immune responses. TLRs recognize conserved motifs found in various pathogens and mediate defense responses. Triggering of the TLR pathway leads to the activation of NF-κB and subsequent regulation of immune and inflammatory genes. The TLRs and members of the IL-1 receptor family share a conserved stretch of approximately 200 amino acids known as the TIR domain. Upon activation, TLRs associate with a number of cytoplasmic adaptor proteins containing TIR domains including MyD88 (myeloid differentiation factor), MAL/TIRAP (MyD88-adaptor-like/TIR-associated protein), TRIF (Toll-receptor-associated activator of interferon), and TRAM (Toll-receptor-associated molecule). This association leads to the recruitment and activation of IRAK1 and IRAK4, which form a complex with TRAF6 to activate TAK1 and IKK. Activation of IKK leads to the degradation of IκB that normally maintains NF-κB inactivity by sequestering it in the cytoplasm.TLR3 functions as a receptor for double-stranded (ds)RNA typically associated with viral infection. It was originally shown to be specifically expressed in dendritic cells of the leukocyte family. TLR3 has also been found in placenta and lung, and can be induced by LPS in a variety of tissues. TLR3 is predominantly localized to early endosomes. Binding of dsRNA, or the analog polyinosine-polycytidylic acid (pIpC), to TLR3 triggers activation of transcription factors NF-κB and IRF3 through the adaptor protein TICAM-1/TRIF. TRIF associates with members of the TRAF family and with RIP that combine to activate NF-κB and IRF3.
Size
100μl(100μg)
Species
Homo Sapiens (Human)
Subcellular Location
Endoplasmic reticulum membrane, Single-pass type I membrane protein, Endosome membrane, Early endosome
This protein 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 receptor is most abundantly expressed in placenta and pancreas, and is restricted to the dendritic subpopulation of the leukocytes. It recognizes dsRNA associated with viral infection, and induces the activation of NF-kappaB and the production of type I interferons. It may thus play a role in host defense against viruses. Use of alternative polyadenylation sites to generate different length transcripts has been noted for this gene.
Key component of innate and adaptive immunity. TLRs (Toll-like receptors) control host immune response against pathogens through recognition of molecular patterns specific to microorganisms. TLR3 is a nucleotide-sensing TLR which is activated by double-stranded RNA, a sign of viral infection. Acts via the adapter TRIF/TICAM1, leading to NF-kappa-B activation, IRF3 nuclear translocation, cytokine secretion and the inflammatory response.
Pathway
Necroptosis Toll-like receptor signaling pathway
Protein Families
Toll-like receptor family
Tissue Specificity
Expressed at high level in placenta and pancreas. Also detected in CD11c+ immature dendritic cells. Only expressed in dendritic cells and not in other leukocytes, including monocyte precursors. TLR3 is the TLR that is expressed most strongly in the brain,
Buffer
Buffer: PBS with 0.02% sodium azide, 50% glycerol, pH7.3.
Format
liquid
Purification
Affinity purification
Purity
Affinity purification
Storage
Upon receipt, store at -20°C or -80°C. Avoid repeated freeze.
Storage Buffer
Store at -20oC or -80oC. Avoid freeze / thaw cycles. Buffer: PBS with 0.02% sodium azide, 50% glycerol, pH7.3.