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Human TLR3 Protein expressed in Escherichia coli (E. coli) - ABIN2667591
Bell, Botos, Hall, Askins, Shiloach, Segal, Davies: The molecular structure of the Toll-like receptor 3 ligand-binding domain. in Proceedings of the National Academy of Sciences of the United States of America 2005
Show all 5 references for ABIN2667591
Mouse (Murine) TLR3 Protein expressed in Baculovirus infected Insect Cells - ABIN2007429
Lafon, Megret, Lafage, Prehaud: The innate immune facet of brain: human neurons express TLR-3 and sense viral dsRNA. in Journal of molecular neuroscience : MN 2006
Show all 4 references for ABIN2007429
Mouse (Murine) TLR3 Protein expressed in Human Cells - ABIN2007431
Johnsen, Nguyen, Ringdal, Tryggestad, Bakke, Lien, Espevik, Anthonsen: Toll-like receptor 3 associates with c-Src tyrosine kinase on endosomes to initiate antiviral signaling. in The EMBO journal 2006
Show all 4 references for ABIN2007431
Study found TLR3 and IFNgamma to play an important role in Hepatitis E pathogenesis. Patients expressing high levels of TLR 3 and robust IFNgamma response are able to recover from the disease; while those with lower expression progress to acute liver failure.
Study clearly demonstrated that the expression of this isoform of TLR3 was a negative regulator of signaling pathways and that it was inducible by type I interferons. Authors also found that this isoform could modulate inflammation in the brain.
TLR3 polymorphisms are unlikely to play a significant role in the development of preeclampsia in the Chinese Han population.
The anti-viral effect of IL-24 (show IL24 Proteins) correlated with caspase-3 (show CASP3 Proteins) activation and could be blocked by a pan-caspase (show CASP3 Proteins) inhibitor and by small interfering RNA (siRNA) directed towards TLR3.
role of TLR3/BAFF axis in IgA class-switch recombination of IgA nephropathy
TLR3 has a role in inducing inflammation in nasopharyngeal carcinoma through EBV-encoded RNA
Findings indicate that melanoma differentiation associated protein-5 (MDA5 (show IFIH1 Proteins)) may serve as a complementary role in the toll (show TLR4 Proteins)-like receptor3 (TLR3) activated suppression of neuroblastoma (show ARHGEF16 Proteins) (NB).
We found that activation of TLR3 signaling could induce the expression of CXCL1 in mesangial cells
Based on the collective findings, we suggest that vIRF2 acts as an activator in PI3K (show PIK3CA Proteins)/Akt (show AKT1 Proteins) pathway.
High TLR3 expression is associated with Inflammatory Bowel Disease.
The results imply that recognition of resident viruses by TLR3 and TLR7 (show TLR7 Proteins) is required for protective immunity during gut (show GUSB Proteins) inflammation.
TRIF (show RNF138 Proteins)-independent pathways can be involved in the downregulation of drug metabolizing enzymes and transporters through TLR4 (show TLR4 Proteins) and 3. JNK (show MAPK8 Proteins)-dependent mechanisms likely mediate this downregulation.
Results show that toll (show TLR4 Proteins)/IL-1 (show IL1A Proteins) domain-containing adaptor inducing IFN-beta (show IFNB1 Proteins) (TRIF (show RNF138 Proteins)) is essential for Toll (show TLR4 Proteins)-like receptors TLR3- and TLR4 (show TLR4 Proteins)-mediated innate immune responses in peritoneal mesothelial cells (PMCs).
during Respiratory syncytial virus infection, respiratory macrophages and dendritic cells mediate the production of IL-33 (show IL33 Proteins) in a TLR-dependent manner
TNFalpha (show TNF Proteins)-blockade stabilizes local airway hyperresponsiveness during TLR3/4-induced exacerbations in murine model of asthma.
Shock wave treatment protects from neuronal degeneration via TLR3 signaling and subsequent TLR4 (show TLR4 Proteins) downregulation in model of ischemic spinal cord injury.
The authors confirmed that the protective effect of poly I:C against enteric infection of mice with Yersinia enterocolitica was dependent on TLR3-mediated TRIF (show RNF138 Proteins) signaling by using TLR3-deficient mice.
The results of the present study indicate that activation of TLR3 by PolyI:C induces the spermatogonial stem cells apoptosis, which implies that viral infection may interfere with the male germ cell development.
dsRNA and TLR3 link the earliest events of mammalian skin wounding to regeneration and suggest potential therapeutic approaches for promoting hair neogenesis.
Data indicate that calgranulin B (S100A9 (show S100A9 Proteins)) is essential for in vivo toll like receptor 3 (TLR3) signaling.
These data demonstrated that TLR2, TLR3 and TLR9 (show TLR9 Proteins) contribute to NF-kappaB (show NFKB1 Proteins) activation in response to porcine epidemic diarrhea virus infection, but not RIG-I (show DDX58 Proteins).
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 Proteins) 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.
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.
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