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Dog (Canine) Monoclonal TLR3 Primary Antibody für FACS, ICC - ABIN4360082
Wen, Peng, Li, Wong: The effect of innate immunity on autoimmune diabetes and the expression of Toll-like receptors on pancreatic islets. in Journal of immunology (Baltimore, Md. : 1950) 2004
Show all 65 Pubmed References
Dog (Canine) Monoclonal TLR3 Primary Antibody für FACS, ICC - ABIN4360084
Evangelista, Castro, Alves, Dias, Souza, Reis, Silva, Castañon, Farias, Juliano, Ferreira: Early IFN-γ production together with decreased expression of TLR3 and TLR9 characterizes EAE development conditional on the presence of myelin. in Autoimmunity 2016
Show all 24 Pubmed References
Dog (Canine) Monoclonal TLR3 Primary Antibody für ELISA - ABIN4248101
Ranjith-Kumar, Miller, Xiong, Russell, Lamb, Santos, Duffy, Cleveland, Park, Bhardwaj, Wu, Russell, Sarisky, Mbow, Kao: Biochemical and functional analyses of the human Toll-like receptor 3 ectodomain. in The Journal of biological chemistry 2007
Show all 21 Pubmed References
Human Polyclonal TLR3 Primary Antibody für FACS, IHC (fro) - ABIN252527
Patole, Gröne, Segerer, Ciubar, Belemezova, Henger, Kretzler, Schlöndorff, Anders: Viral double-stranded RNA aggravates lupus nephritis through Toll-like receptor 3 on glomerular mesangial cells and antigen-presenting cells. in Journal of the American Society of Nephrology : JASN 2005
Show all 14 Pubmed References
Human Monoclonal TLR3 Primary Antibody für FACS, IF - ABIN531989
Wong, Cheung, Ip, Lam: Intracellular signaling mechanisms regulating toll-like receptor-mediated activation of eosinophils. in American journal of respiratory cell and molecular biology 2007
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Human Monoclonal TLR3 Primary Antibody für FACS, IF - ABIN2191972
Matsumoto, Kikkawa, Kohase, Miyake, Seya: Establishment of a monoclonal antibody against human Toll-like receptor 3 that blocks double-stranded RNA-mediated signaling. in Biochemical and biophysical research communications 2002
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Human Monoclonal TLR3 Primary Antibody für FACS, IF - ABIN2191974
Oshiumi, Matsumoto, Funami, Akazawa, Seya: TICAM-1, an adaptor molecule that participates in Toll-like receptor 3-mediated interferon-beta induction. in Nature immunology 2003
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Human Monoclonal TLR3 Primary Antibody für FACS, IF - ABIN2191973
Matsumoto, Funami, Tanabe, Oshiumi, Shingai, Seto, Yamamoto, Seya: Subcellular localization of Toll-like receptor 3 in human dendritic cells. in Journal of immunology (Baltimore, Md. : 1950) 2003
Show all 6 Pubmed References
Human Polyclonal TLR3 Primary Antibody für ICC, IF - ABIN4360085
Hsieh, Chang, Chen, Li, Chuang, Yu, Cheung, Chen, Maa, Leu: The inducible nitric-oxide synthase (iNOS)/Src axis mediates Toll-like receptor 3 tyrosine 759 phosphorylation and enhances its signal transduction, leading to interferon-β synthesis in macrophages. in The Journal of biological chemistry 2014
Show all 6 Pubmed References
Mouse (Murine) Polyclonal TLR3 Primary Antibody für IF (p), IHC (p) - ABIN686617
Zhu, Meng, Jiang, Xu, Wang, Han, Lu: Overexpression of toll-like receptor 3 in spleen is associated with experimental arthritis in rats. in Scandinavian journal of immunology 2012
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Functional variations in the expression of TLR found in blood and hypertrophied fat depots, namely decreased TLR3 in lymphocytes and inflamed adipocytes, are linked to metabolic inflammation.
study reveals that upregulation of PGES via TLR3 is critical for BM-MSCs-mediated immunosuppression by PGE2 secretion via the COX-2/PGE2 pathway.
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 Notch1/2 in CD14+ 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) can modulate specific cutaneous inflammatory responses and that the decrease in cutaneous REG3A exacerbates toll-like receptor 3 (TLR3)-mediated inflammation in diabetic skin wounds.
These data indicate a novel role of the TLR3-TICAM-1 pathway in controlling miR-21 levels in extracellular vesicles.
The TLR3.rs3775290 "CC" genotype was associated with hepatitis C virus chronicity, while the TLR9 gene may not play a major role in hepatitis C virus infection.
CYLD inhibits post-transcriptional regulation of RIG-I and MDA5 expression following TLR3 activation in MCs. CYLD 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.
These results demonstrate that histamine up-regulates the expression of TLR3 and secretion of IL-13 and MCP-1 in mast cells, thus identifying a new mechanism for the histamine inducing allergic response.
Reduced response of NK cells to TLR3 stimulation in children with recurrent infections has been observed.
Using hepatocyte-based culture models for Hepatitis C virus (HCV) infection, we found a portion of HCV dsRNA intermediates to be released from infected cells in extracellular vesicles, which reduces activation of toll-like receptor 3.
the association between TLR3, TLR4 variants and nine IL-6 polymorphisms, and response to anti-viral treatment during hepatitis C infection.
results suggest that patients with Toll-like receptor 3 gene polymorphisms could be susceptible to periapical pathosis.
Studied associations of 12 single nucleotide polymorphisms (SNPs) within toll like receptor genes (TLR2, TLR3, TLR4, and TLR9) and genetic predisposition to neonatal severe hepatitis. Found certain SNPS were associated with prognosis of neonatal severe hepatitis.
The current study suggests that TLR3 signaling induces CCL5 expression via NF-kappaB and IRF3 in bile duct cells, and this pathway may be involved in the pathogenesis of BA.
The down regulation of TRIF, TLR3, and mitochondrial antiviral signaling protein (MAVS) expressions in chronic hepatitis C correlates with the disease severity and the outcome of hepatitis C virus infection
These data indicate that sepsis-induced cardiac dysfunction requires presence of TLR3 and TLR9 and may be linked to histone-induced damage of cardiomyocytes.
Pregnant mice lacking TLR3 in both maternal systemic and placental cells were completely resistant to the hypertension, proteinuria, fetal demise, endothelial dysfunction, splenomegaly, and increases in pro-inflammatory immune cells induced by TLR3 activation.
results indicate that TLR3 is the primary molecule which modulates the activation and function of NK cells during the course of Schistosoma japonicum infection in C57BL/6 mice
This study demonstrates that the synergistic effect between TLR4 and TLR3 in macrophages is an important determinant in acute lung injury and, more importantly, that TLR3 up-regulation is dependent on TLR4-MyD88-NF-kappaB 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(+) 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 pathway inhibits polyposis through suppression of c-Myc expression and supports long survival in Apc (Min/+) mice.
PolyI:C targeted Toll-like receptor 3 with minimal effect on the mitochondrial antiviral-signaling protein 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 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 is a critical component of the IRF1 and IRF2 transcriptional machinery that regulates Tlr3 gene expression.
the JAK-STAT 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 pathways.
These results suggest that testicular innate immune responses to pathogens caused by nano-TiO2 may be involved in the regulatory mechanisms of TAM/TLR3 signaling in testicular Sertoli cells.
findings report that RKIP preferentially regulates the TLR3-mediated immune response in macrophages; phosphorylation of RKIP serine 109 is required for RKIP 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 activation in a manner partially dependent on miR-155.
Primary tumor-derived exosomal RNAs, which are enriched in small nuclear RNAs, activate TLR3 in lung epithelial cells, consequently inducing chemokine secretion in the lung and promoting neutrophil recruitment.
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, or MyD88 fail to undergo L. major-induced autophagy. (TLR = Toll-like receptor; Unc93b1 = unc-93 homolog B1; MyD88 = myeloid differentiation primary response gene 88)
RIG-I and TLR3 interact with the pseudoknot of Porcine Reproductive and Respiratory Syndrome Virus 3' untranslated regions. Both RIG-I and TLR3 are required for the pseudoknot to induce interferon response.
These data demonstrated that TLR2, TLR3 and TLR9 contribute to NF-kappaB activation in response to porcine epidemic diarrhea virus infection, but not RIG-I.
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 inducing capability.
5 known non-synonymous single nucleotide polymorphisms (SNPs) were characterized in the coding sequences of the porcine TLR3 gene.
molecular sequence characterization and expression in co-infection with influenza virus and Bordetella bronchiseptica
Activation of porcine TLR3 signaling is important in stimulating effective responses to PRRSV infection.
Targeting the Mincle and TLR3 receptor using the dual agonist cationic adjuvant formulation 9 (CAF09) induces humoral and polyfunctional memory T cell responses in calves
On day 104 of pregnancy, mRNA expression of TLRs 3 and 8, as well as that of TLRs 7 and 9, was high in the spleen of fetuses from Neospora caninum-infected heifers. Gene expression levels of endosomal TLRs were also detectable in the placenta and the maternal caruncle from infected heifers, being TLRs 3, 7 and 8 particularly upregulated, mostly in the caruncle.
The results from this study demonstrate that expression of at least TLR3, TLR7 and TLR8 is stimulated upon bovine alpha-herpesvirus infection of the brain.
Comparative sequence analysis revealed a total of 139 polymorphisms, which include single-nucleotide polymorphisms and insertion-deletion polymorphisms.
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-/- 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