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Dog (Canine) Monoclonal TLR3 Primary Antibody for 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
Dog (Canine) Monoclonal TLR3 Primary Antibody for 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 64 Pubmed References
Dog (Canine) Monoclonal TLR3 Primary Antibody for 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 for FACS - ABIN4360083
Funami, Matsumoto, Oshiumi, Akazawa, Yamamoto, Seya: The cytoplasmic 'linker region' in Toll-like receptor 3 controls receptor localization and signaling. in International immunology 2004
Show all 25 Pubmed References
Human Polyclonal TLR3 Primary Antibody for 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 13 Pubmed References
Human Monoclonal TLR3 Primary Antibody for FACS, IF - ABIN2191973
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
Show all 6 Pubmed References
Human Monoclonal TLR3 Primary Antibody for FACS, IF - ABIN2191972
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
Show all 6 Pubmed References
Human Monoclonal TLR3 Primary Antibody for FACS, IF - ABIN2191974
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 for 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 for 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
Show all 3 Pubmed References
These data demonstrate that in the absence of HBsAg, hepatic hepatitis B virus replication leads to Tlr3-dependent interferon (show IFNA Antibodies) responses in non-parenchymal liver cells.
Study found that the astrocytic TLR3-mediated cytokine expression profile is modulated by prostaglandin, and NF-kappaB (show NFKB1 Antibodies), ERK1/2 (show MAPK1/3 Antibodies) and GSK-3beta (show GSK3b Antibodies) are involved in the modulatory mechanism. These results suggest that pathological conditions with increased COX (show COX8A Antibodies) activity can neuroimmunologically alter neuron-glia interaction.
Activation of TLR3 and TLR4 (show TLR4 Antibodies) stimulated the expression of HIF-1 (show HIF1A Antibodies) through NF-kappaB (show NFKB1 Antibodies) in oral squamous cell carcinoma
The present study investigated the effects of vitamin D3 on the expression of TLR3, TLR7 (show TLR7 Antibodies), and TLR9 (show TLR9 Antibodies) in Systemic lupus erythematosus patients.
TLR3 or TLR4 (show TLR4 Antibodies) activation of mesenchymal stem cells increases Treg cell induction via the Notch (show NOTCH1 Antibodies) 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 Antibodies)) production and promote invasiveness of IECs. (TLR3 = toll-like receptor 3; CXCL10 (show CXCL10 Antibodies) = chemokine (show CCL1 Antibodies) [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 Antibodies) 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 Antibodies)), and decreased anti-oxidative response.
Ligand-driven triggering of TLR-3, -4, NOD2 (show NOD2 Antibodies), and DC-SIGN (show CD209 Antibodies), despite reducing viral replication, markedly increased the capacity of infected dendritic cells to stimulate HIV-specific cytotoxic T-cells.
This study establishes a correlation between TLR-3 and TLR-9 (show TLR9 Antibodies) 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 Antibodies) is a critical component of the IRF1 (show IRF1 Antibodies) and IRF2 (show IRF2 Antibodies) transcriptional machinery that regulates Tlr3 gene expression.
the JAK (show JAK3 Antibodies)-STAT (show STAT1 Antibodies) 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 Antibodies) 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 Antibodies)/TLR3 signaling in testicular Sertoli cells.
findings report that RKIP (show PEBP1 Antibodies) preferentially regulates the TLR3-mediated immune response in macrophages; phosphorylation of RKIP (show PEBP1 Antibodies) serine 109 is required for RKIP (show PEBP1 Antibodies) 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 Antibodies) activation in a manner partially dependent on miR (show MLXIP Antibodies)-155.
Primary tumor-derived exosomal RNAs, which are enriched in small nuclear RNAs, activate TLR3 in lung epithelial cells, consequently inducing chemokine (show CCL1 Antibodies) 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 (show UNC93B1 Antibodies), or MyD88 (show MYD88 Antibodies) fail to undergo L. major-induced autophagy. (TLR = Toll (show TLR4 Antibodies)-like receptor; Unc93b1 (show UNC93B1 Antibodies) = unc-93 (show UNC93B1 Antibodies) homolog B1; MyD88 (show MYD88 Antibodies) = myeloid differentiation primary response gene 88 (show MYD88 Antibodies))
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 Antibodies), TLR3 and TLR9 (show TLR9 Antibodies) contribute to NF-kappaB (show NFKB1 Antibodies) activation in response to porcine epidemic diarrhea virus infection, but not RIG-I (show DDX58 Antibodies).
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 Antibodies) 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 Antibodies) and TLR8 (show TLR8 Antibodies) is stimulated upon bovine alpha-herpesvirus infection of the brain.
TLR2 (show TLR2 Antibodies), 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 Antibodies)-/- 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