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Human TLR3 ELISA Kit for Sandwich ELISA - ABIN417426
Yang, Xie, Deng, Qin: Expression of soluble Toll-like receptors in pleural effusions. in Chinese medical journal 2010
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TLR3 or TLR4 (show TLR4 ELISA Kits) activation of mesenchymal stem cells increases Treg cell induction via the Notch (show NOTCH1 ELISA Kits) pathway
Data suggest that, unlike non-metastatic intestinal epithelial cells (IECs), metastatic IECs express TLR3 and that TLR3 agonists induce inflammatory cytokine (CXCL10 (show CXCL10 ELISA Kits)) production and promote invasiveness of IECs. (TLR3 = toll-like receptor 3; CXCL10 (show CXCL10 ELISA Kits) = chemokine (show CCL1 ELISA Kits) [C-X-C motif] ligand 10 protein)
TLR3-activated macrophages release exosomes that contain anti-HCV microRNA (miRNA)-29 family member
homozygous IFITM3 (show IFITM3 ELISA Kits) CC and TLR3 CC genotypes showed significant independent associations with higher death risks in H7N9/H1N1pdm09 influenza in a large Chinese cohort
TLR3 activation can induce metabolic reprogramming in a pharyngeal cancer cell line, leading to increased aerobic glycolysis, cell migration, elevated levels of reactive oxidative species (ROS (show ROS1 ELISA Kits)), and decreased anti-oxidative response.
Ligand-driven triggering of TLR-3, -4, NOD2 (show NOD2 ELISA Kits), and DC-SIGN (show CD209 ELISA Kits), despite reducing viral replication, markedly increased the capacity of infected dendritic cells to stimulate HIV-specific cytotoxic T-cells.
Since mumps virus SH coimmunoprecipitated with tumor necrosis factor receptor 1 (TNFR1 (show TNFRSF1A ELISA Kits)), RIP1, and IRAK1 (show IRAK1 ELISA Kits), we hypothesize that SH exerts its NF-kappaB (show NFKB1 ELISA Kits) activation inhibitory function by interacting with TNFR1 (show TNFRSF1A ELISA Kits), interleukin-1 receptor type 1 (IL-1R1), and TLR3 complexes in the plasma membrane of infected cells.
Primary tumor-derived exosomal RNAs, which are enriched in small nuclear RNAs, activate TLR3 in lung epithelial cells, consequently inducing chemokine (show CCL1 ELISA Kits) secretion in the lung and promoting neutrophil recruitment.
the L412F polymorphism in the TLR3 gene could be a genetic risk factor for the development of human cytomegalovirus disease
Studied Toll-like receptor 3 (TLR3) mutations in a cohort of 11 adult Italian viral encephalitis patients.
This study establishes a correlation between TLR-3 and TLR-9 (show TLR9 ELISA Kits) expression with the development of EAE. In addition, evidence of a role for the myelin peptide in targeting the innate inflammatory response to the CNS is presented.
Data show that HCFC2 (show HCFC2 ELISA Kits) is a critical component of the IRF1 (show IRF1 ELISA Kits) and IRF2 (show IRF2 ELISA Kits) transcriptional machinery that regulates Tlr3 gene expression.
the JAK (show JAK3 ELISA Kits)-STAT (show STAT1 ELISA Kits) pathway provides a cytokine rheostat mechanism, which enables macrophages to fine-tune their responses to multiple, temporally separated infection events involving the TLR3 and TLR7 (show TLR7 ELISA Kits) pathways.
These results suggest that testicular innate immune responses to pathogens caused by nano-TiO2 may be involved in the regulatory mechanisms of TAM (show CCNA1 ELISA Kits)/TLR3 signaling in testicular Sertoli cells.
findings report that RKIP (show PEBP1 ELISA Kits) preferentially regulates the TLR3-mediated immune response in macrophages; phosphorylation of RKIP (show PEBP1 ELISA Kits) serine 109 is required for RKIP (show PEBP1 ELISA Kits) to promote TLR3-mediated signaling and inflammation
Furthermore, Leishmania RNA virus 1-induced TLR-3 activation promoted parasite persistence by enhancing macrophage survival through Akt (show AKT1 ELISA Kits) activation in a manner partially dependent on miR (show MLXIP ELISA Kits)-155.
Autophagy contributes to macrophage resistance to Leishmania major. Data, including data from studies in knockout mice, suggest a key resistance mechanism involves endosomal signaling via Tlr3/7/9 in macrophages; macrophages deficient for Tlr3/7/9, Unc93b1 (show UNC93B1 ELISA Kits), or MyD88 (show MYD88 ELISA Kits) fail to undergo L. major-induced autophagy. (TLR = Toll (show TLR4 ELISA Kits)-like receptor; Unc93b1 (show UNC93B1 ELISA Kits) = unc-93 (show UNC93B1 ELISA Kits) homolog B1; MyD88 (show MYD88 ELISA Kits) = myeloid differentiation primary response gene 88 (show MYD88 ELISA Kits))
Our study reveals a novel mechanism of TLR3 in regulation of dendritic morphology and provides an explanation for how environmental factors influence mental health.
LUBAC components control TLR3-mediated innate immunity, thereby preventing development of immunodeficiency and autoinflammation.
These data demonstrated that TLR2 (show TLR2 ELISA Kits), TLR3 and TLR9 (show TLR9 ELISA Kits) contribute to NF-kappaB (show NFKB1 ELISA Kits) activation in response to porcine epidemic diarrhea virus infection, but not RIG-I (show DDX58 ELISA Kits).
TLR3 is regulated differentially by different genotype 1 PRRSV strains and this seems to be related apparently to the replication levels of each strain, as well as, to the TNF-alpha (show TNF ELISA Kits) inducing capability.
5 known non-synonymous single nucleotide polymorphisms (SNPs) were characterized in the coding sequences of the porcine TLR3 gene.
Activation of porcine TLR3 signaling is important in stimulating effective responses to PRRSV infection.
The results from this study demonstrate that expression of at least TLR3, TLR7 (show TLR7 ELISA Kits) and TLR8 (show TLR8 ELISA Kits) is stimulated upon bovine alpha-herpesvirus infection of the brain.
TLR2 (show TLR2 ELISA Kits), 3, 4, and 8 mRNA expression is strongly upregulated and correlates with the progression of atherosclerosis in the aorta. Fluvastatin significantly inhibited this progress and reduced inflammation via TLR downregulation.
18 SNPs of TLR3 were observed and only 4 polymorphic positions were detected in the domestic breeds and 14 non-synonymous substitutions were observed, most of them in the LRR molecules.
Differential gene expression following TLR stimulation in rag1 (show RAG1 ELISA Kits)-/- mutant zebrafish tissues and morphological descriptions of lymphocyte-like cell populations
Binding energy (BE) calculation using MM/PBSA method from the TLR3- and TLR22-ligand complexes revealed an adequate binding affinity between TLR22-monomer and dsRNA as like as TLR3-dimer-dsRNA complex.
Full-length tlr3 was functionally characterized.
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 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.
toll-like receptor 3
, toll-like receptor 3-like
, toll-like receptor 3 variant 1