External Ids for TLR7 Gene
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 predominantly expressed in lung, placenta, and spleen, and lies in close proximity to another family member, TLR8, on chromosome X. [provided by RefSeq, Jul 2008]
GeneCards Summary for TLR7 Gene
TLR7 (Toll-Like Receptor 7) is a Protein Coding gene. Diseases associated with TLR7 include anogenital venereal wart and congenital heart block. Among its related pathways are NF-KappaB Family Pathway and NF-KappaB Family Pathway. GO annotations related to this gene include drug binding and single-stranded RNA binding. An important paralog of this gene is TLR6.
UniProtKB/Swiss-Prot for TLR7 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. TLR7 is a nucleotide-sensing TLR which is activated by single-stranded RNA. Acts via MYD88 and TRAF6, leading to NF-kappa-B activation, cytokine secretion and the inflammatory response (By similarity).
Toll-like receptors (TLRs) are single transmembrane cell-surface receptors, which have a key role in the innate immune system. TLRs generally exist as homodimers (although TLR2-TLR6 heterodimers have been reported) and are found on immune cells such as macrophages, B lymphocytes and mast cells. Toll-like receptors are activated by molecules associated with biological threat and are highly specific towards evolutionary conserved entities on microbes, such as bacterial cell-surface lipopolysaccharides, flagella and unmethylated CpG islands. It has been suggested that some toll-like receptors may have endogenous ligands, such as Hsp60 and fibrinogen, and this has promoted speculation that endogenous toll-like receptor activators may have a pathological role in autoimmune disease. Activation of toll-like receptors initiates downstream signaling cascades, initially via the adapter molecules MyD88, Trap, Trif and Tram, which converge on the PI 3-K and NF-kappaB pathways and regulate intracellular kinases and gene expression. This can stimulate an inflammatory and/or antigen-specific immune response. The signaling cascade coupled to toll-like receptor activation is very similar to that of interleukin-1 receptor (IL-1R) activation.