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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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Data suggest that, unlike non-metastatic intestinal epithelial cells (IECs), metastatic IECs express TLR3 and that TLR3 agonists induce inflammatory cytokine (CXCL10 (显示 CXCL10 ELISA试剂盒)) production and promote invasiveness of IECs. (TLR3 = toll-like receptor 3; CXCL10 (显示 CXCL10 ELISA试剂盒) = chemokine (显示 CCL1 ELISA试剂盒) [C-X-C motif] ligand 10 protein)
TLR3-activated macrophages release exosomes that contain anti-HCV microRNA (miRNA)-29 family member
homozygous IFITM3 (显示 IFITM3 ELISA试剂盒) 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 (显示 ROS1 ELISA试剂盒)), and decreased anti-oxidative response.
Ligand-driven triggering of TLR-3, -4, NOD2 (显示 NOD2 ELISA试剂盒), and DC-SIGN (显示 CD209 ELISA试剂盒), 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 (显示 TNFRSF1A ELISA试剂盒)), RIP1, and IRAK1 (显示 IRAK1 ELISA试剂盒), we hypothesize that SH exerts its NF-kappaB (显示 NFKB1 ELISA试剂盒) activation inhibitory function by interacting with TNFR1 (显示 TNFRSF1A ELISA试剂盒), 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 (显示 CCL1 ELISA试剂盒) 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.
Report PD-1 (显示 PDCD1 ELISA试剂盒)/PD-L1 (显示 CD274 ELISA试剂盒) and TLR3 expression in malignant pleural mesotheliomas as possible tests for selection patients who could benefit from immunotherapy.
the JAK (显示 JAK3 ELISA试剂盒)-STAT (显示 STAT1 ELISA试剂盒) 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 (显示 TLR7 ELISA试剂盒) pathways.
These results suggest that testicular innate immune responses to pathogens caused by nano-TiO2 may be involved in the regulatory mechanisms of TAM (显示 CCNA1 ELISA试剂盒)/TLR3 signaling in testicular Sertoli cells.
findings report that RKIP (显示 PEBP1 ELISA试剂盒) preferentially regulates the TLR3-mediated immune response in macrophages; phosphorylation of RKIP (显示 PEBP1 ELISA试剂盒) serine 109 is required for RKIP (显示 PEBP1 ELISA试剂盒) 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 (显示 AKT1 ELISA试剂盒) activation in a manner partially dependent on miR (显示 MLXIP ELISA试剂盒)-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 (显示 UNC93B1 ELISA试剂盒), or MyD88 (显示 MYD88 ELISA试剂盒) fail to undergo L. major-induced autophagy. (TLR = Toll (显示 TLR4 ELISA试剂盒)-like receptor; Unc93b1 (显示 UNC93B1 ELISA试剂盒) = unc-93 (显示 UNC93B1 ELISA试剂盒) homolog B1; MyD88 (显示 MYD88 ELISA试剂盒) = myeloid differentiation primary response gene 88 (显示 MYD88 ELISA试剂盒))
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.
results reveal a novel CD40 (显示 CD40 ELISA试剂盒)-dependent regulation of PD-L1 (显示 CD274 ELISA试剂盒) trafficking induced upon TLR3 signaling that dictates its inhibitory activity.
This study reveals novel insights into the pathophysiology of epilepsy and the contribution of TLR3 to disease progression.
These data demonstrated that TLR2 (显示 TLR2 ELISA试剂盒), TLR3 and TLR9 (显示 TLR9 ELISA试剂盒) contribute to NF-kappaB (显示 NFKB1 ELISA试剂盒) activation in response to porcine epidemic diarrhea virus infection, but not RIG-I (显示 DDX58 ELISA试剂盒).
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 (显示 TNF ELISA试剂盒) 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 (显示 TLR7 ELISA试剂盒) and TLR8 (显示 TLR8 ELISA试剂盒) is stimulated upon bovine alpha-herpesvirus infection of the brain.
TLR2 (显示 TLR2 ELISA试剂盒), 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 (显示 RAG1 ELISA试剂盒)-/- 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