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抗Human TLR3 抗体:
抗Mouse (Murine) TLR3 抗体:
抗Rat (Rattus) TLR3 抗体:
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
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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
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
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
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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
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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
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Human Monoclonal TLR3 Primary Antibody for FACS, IF - ABIN2191972
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
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Bird (Avian) Polyclonal TLR3 Primary Antibody for FACS, IHC (p) - ABIN4360080
Kuzemtseva, de la Torre, Martín, Soldevila, Ait-Ali, Mateu, Darwich: Regulation of toll-like receptors 3, 7 and 9 in porcine alveolar macrophages by different genotype 1 strains of porcine reproductive and respiratory syndrome virus. in Veterinary immunology and immunopathology 2014
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we report that autophagy is associated with apoptosis processes, involving LC3 (显示 MAP1LC3A 抗体) and TRIF (显示 TRIM69 抗体)-colocation in human HCC (显示 FAM126A 抗体) cells. Regulation of autophagy and the TLR3-TRIF (显示 TRIM69 抗体) pathway may be effective in the treatment of liver cancer.
Polymorphism of CD209 (显示 CD209 抗体) and TLR3 genes in populations of North Eurasia
TLR3-activated signaling enhanced the therapeutic effects of human umbilical cord-derived mesenchymal stem cells in a mouse model of colitis
the TLR3 Leu412Phe CC genotype is independently associated with severity of hepatitis C recurrence after LT.
These data demonstrate that in the absence of HBsAg, hepatic hepatitis B virus replication leads to Tlr3-dependent interferon (显示 IFNA 抗体) responses in non-parenchymal liver cells.
Study found that the astrocytic TLR3-mediated cytokine expression profile is modulated by prostaglandin, and NF-kappaB (显示 NFKB1 抗体), ERK1/2 (显示 MAPK1/3 抗体) and GSK-3beta (显示 GSK3b 抗体) are involved in the modulatory mechanism. These results suggest that pathological conditions with increased COX (显示 COX8A 抗体) activity can neuroimmunologically alter neuron-glia interaction.
Activation of TLR3 and TLR4 (显示 TLR4 抗体) stimulated the expression of HIF-1 (显示 HIF1A 抗体) through NF-kappaB (显示 NFKB1 抗体) in oral squamous cell carcinoma
The present study investigated the effects of vitamin D3 on the expression of TLR3, TLR7 (显示 TLR7 抗体), and TLR9 (显示 TLR9 抗体) in Systemic lupus erythematosus patients.
TLR3 or TLR4 (显示 TLR4 抗体) activation of mesenchymal stem cells increases Treg cell induction via the Notch (显示 NOTCH1 抗体) pathway
Data suggest that, unlike non-metastatic intestinal epithelial cells (IECs), metastatic IECs express TLR3 and that TLR3 agonists induce inflammatory cytokine (CXCL10 (显示 CXCL10 抗体)) production and promote invasiveness of IECs. (TLR3 = toll-like receptor 3; CXCL10 (显示 CXCL10 抗体) = chemokine (显示 CCL1 抗体) [C-X-C motif] ligand 10 protein)
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 (显示 TLR9 抗体) 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 (显示 HCFC2 抗体) is a critical component of the IRF1 (显示 IRF1 抗体) and IRF2 (显示 IRF2 抗体) transcriptional machinery that regulates Tlr3 gene expression.
the JAK (显示 JAK3 抗体)-STAT (显示 STAT1 抗体) 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 (显示 TLR7 抗体) pathways.
These results suggest that testicular innate immune responses to pathogens caused by nano-TiO2 may be involved in the regulatory mechanisms of TAM (显示 CCNA1 抗体)/TLR3 signaling in testicular Sertoli cells.
findings report that RKIP (显示 PEBP1 抗体) preferentially regulates the TLR3-mediated immune response in macrophages; phosphorylation of RKIP (显示 PEBP1 抗体) serine 109 is required for RKIP (显示 PEBP1 抗体) 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 (显示 AKT1 抗体) activation in a manner partially dependent on miR (显示 MLXIP 抗体)-155.
Primary tumor-derived exosomal RNAs, which are enriched in small nuclear RNAs, activate TLR3 in lung epithelial cells, consequently inducing chemokine (显示 CCL1 抗体) 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 (显示 UNC93B1 抗体), or MyD88 (显示 MYD88 抗体) fail to undergo L. major-induced autophagy. (TLR = Toll (显示 TLR4 抗体)-like receptor; Unc93b1 (显示 UNC93B1 抗体) = unc-93 (显示 UNC93B1 抗体) homolog B1; MyD88 (显示 MYD88 抗体) = myeloid differentiation primary response gene 88 (显示 MYD88 抗体))
Our study reveals a novel mechanism of TLR3 in regulation of dendritic morphology and provides an explanation for how environmental factors influence mental health.
These data demonstrated that TLR2 (显示 TLR2 抗体), TLR3 and TLR9 (显示 TLR9 抗体) contribute to NF-kappaB (显示 NFKB1 抗体) activation in response to porcine epidemic diarrhea virus infection, but not RIG-I (显示 DDX58 抗体).
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 (显示 TNF 抗体) 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 (显示 TLR7 抗体) and TLR8 (显示 TLR8 抗体) is stimulated upon bovine alpha-herpesvirus infection of the brain.
TLR2 (显示 TLR2 抗体), 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 (显示 RAG1 抗体)-/- 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