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We report a significant association between TLR3 L412F and persistent clinical disease in two cohorts of Irish and American Caucasians with pulmonary sarcoidosis. This study identifies defective TLR3 function as a previously unidentified factor in persistent clinical disease in pulmonary sarcoidosis and reveals TLR3 L412F as a candidate biomarker.
Data indicate that trigeminal ganglion (TG) neurons are vulnerable to HSV-1 because they require preemptive stimulation of the Toll-like receptor 3 (TLR3) to induce antiviral immunity.
These variations in the TLR3mediated signaling pathway molecules suggested that oxidative stress may be a key regulator for TLR3 activation during RSV infection
In conclusion, we demonstrated that EV71 infection induced elevated expressions of TLR3/4 and Notch1 (zeige NOTCH1 Proteine)/2 in CD14 (zeige NDUFA2 Proteine)+ monocytes.
Increased TLR3 expression in acute exacerbations of chronic obstructive pulmonary disease patients is associated with declining lung function
Data show that regenerating family member 3 alpha protein (REG3A (zeige REG3A Proteine)) can modulate specific cutaneous inflammatory responses and that the decrease in cutaneous REG3A (zeige REG3A Proteine) exacerbates toll-like receptor 3 (TLR3)-mediated inflammation in diabetic skin wounds.
These data indicate a novel role of the TLR3-TICAM-1 (zeige TICAM1 Proteine) pathway in controlling miR (zeige MLXIP Proteine)-21 levels in extracellular vesicles.
The TLR3.rs3775290 "CC" genotype was associated with hepatitis C virus chronicity, while the TLR9 (zeige TLR9 Proteine) gene may not play a major role in hepatitis C virus infection.
CYLD (zeige CYLD Proteine) inhibits post-transcriptional regulation of RIG-I (zeige DDX58 Proteine) and MDA5 (zeige IFIH1 Proteine) expression following TLR3 activation in MCs (zeige SMCP Proteine). CYLD (zeige CYLD Proteine) may be involved in the pathogenesis of CKD
TLR2 up-regulation and TLR3 down-regulation occur in doxorubicin-treated patients who develop heart dysfunction. This may suggest a predictive role of TLR2-TLR3 imbalance in doxorubicin-induced heart failure.
This study demonstrates that the synergistic effect between TLR4 (zeige TLR4 Proteine) and TLR3 in macrophages is an important determinant in acute lung injury and, more importantly, that TLR3 up-regulation is dependent on TLR4 (zeige TLR4 Proteine)-MyD88 (zeige MYD88 Proteine)-NF-kappaB (zeige NFKB1 Proteine) signaling.
Results provide evidence that TLR3 signaling contributes to the dengue virus-induced increase in microglial migration.
this study shows that Tlr3 in nasal CD103 (zeige ITGAE Proteine)(+) dendritic cells is involved in immunoglobulin A production
these data suggest that TLR3 promotes the clearance of Cm during early and mid-stages of genital tract infection, and that loss of TLR3 is detrimental in the development hydrosalpinx.
TLR3 deficiency in Tlr3 KO mice suppressed the development of chronic contact hypersensitivity reactions, suggesting that TLR3 signaling may participate in the pathogenesis of atopic dermatitis.
The TLR3/TICAM-1 (zeige TICAM1 Proteine) pathway inhibits polyposis through suppression of c-Myc (zeige MYC Proteine) expression and supports long survival in Apc (zeige APC Proteine) (Min/+) mice.
PolyI:C targeted Toll-like receptor 3 with minimal effect on the mitochondrial antiviral-signaling protein (zeige MAVS Proteine) pathway.
determined whether the depletion of TLR3 modulated hepatic injury in mice and further aimed to provide mechanistic insights into the TLR3-mediated modulation of diet-induced hepatic inflammation and fat accumulation.
TLR3 signaling contributes to Wallerian degeneration after peripheral nerve injury by affecting Schwann cell activation.
This study establishes a correlation between TLR-3 and TLR-9 (zeige TLR9 Proteine) 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.
RIG-I (zeige DDX58 Proteine) and TLR3 interact with the pseudoknot of Porcine Reproductive and Respiratory Syndrome Virus 3' untranslated regions. Both RIG-I (zeige DDX58 Proteine) and TLR3 are required for the pseudoknot to induce interferon (zeige IFNA Proteine) response.
These data demonstrated that TLR2, TLR3 and TLR9 (zeige TLR9 Proteine) contribute to NF-kappaB (zeige NFKB1 Proteine) activation in response to porcine epidemic diarrhea virus infection, but not RIG-I (zeige DDX58 Proteine).
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 (zeige TNF Proteine) 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 (zeige TLR7 Proteine) and TLR8 (zeige TLR8 Proteine) is stimulated upon bovine alpha-herpesvirus infection of the brain.
TLR2, 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 (zeige RAG1 Proteine)-/- 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