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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 - 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
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
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 - 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
Show all 6 Pubmed References
Human Monoclonal TLR3 Primary Antibody for 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
Show all 6 Pubmed References
Human Monoclonal TLR3 Primary Antibody for 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 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
Dog (Canine) Monoclonal TLR3 Primary Antibody for FACS, IP - ABIN2479738
Campbell: Osteomalacia: diagnosis and management. in British journal of hospital medicine 1991
Show all 4 Pubmed References
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.
Since mumps virus SH coimmunoprecipitated with tumor necrosis factor receptor 1 (TNFR1 (show TNFRSF1A Antibodies)), RIP1 (show UQCRFS1 Antibodies), and IRAK1 (show IRAK1 Antibodies), we hypothesize that SH exerts its NF-kappaB (show NFKB1 Antibodies) activation inhibitory function by interacting with TNFR1 (show TNFRSF1A Antibodies), interleukin-1 receptor type 1 (show IL-1R1 Antibodies) (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 (show CCL1 Antibodies) 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 (show PDCD1 Antibodies)/PD-L1 (show CD274 Antibodies) and TLR3 expression in malignant pleural mesotheliomas as possible tests for selection patients who could benefit from immunotherapy.
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.
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.
results reveal a novel CD40 (show CD40 Antibodies)-dependent regulation of PD-L1 (show CD274 Antibodies) 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.
the activation of TLR3 promotes the loss of RGCs and their axons by elevating Rtca (show RTCD1 Antibodies) levels in the retina. Also, the results presented in this study show that Rtca (show RTCD1 Antibodies) regulates JNK3 (show MAPK10 Antibodies) expression in the retina.
identify iNOS (show NOS2 Antibodies)/NO as an integral component of IFN-beta (show IFNB1 Antibodies) production in response to dsRNA in hepatocytes in a pathway that involves the coordinated activities of TLR3/Trif (show RNF138 Antibodies) and PKR (show EIF2AK2 Antibodies)
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