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anti-Human TLR3 Antikörper:
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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 - 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 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 - 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 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
Show all 6 Pubmed References
Human Monoclonal TLR3 Primary Antibody für 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 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
Bird (Avian) Polyclonal TLR3 Primary Antibody für 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
Show all 4 Pubmed References
CYLD (zeige CYLD Antikörper) inhibits post-transcriptional regulation of RIG-I (zeige DDX58 Antikörper) and MDA5 (zeige IFIH1 Antikörper) expression following TLR3 activation in MCs (zeige SMCP Antikörper). CYLD (zeige CYLD Antikörper) 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 (zeige IL13 Antikörper) and MCP-1 (zeige CCL2 Antikörper) 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 (zeige TLR4 Antikörper) variants and nine IL-6 (zeige IL6 Antikörper) 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 (zeige TLR4 Antikörper) like receptor genes (TLR2, TLR3, TLR4 (zeige TLR4 Antikörper), and TLR9 (zeige TLR9 Antikörper)) 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 (zeige CCL5 Antikörper) expression via NF-kappaB (zeige NFKB1 Antikörper) and IRF3 (zeige IRF3 Antikörper) in bile duct cells, and this pathway may be involved in the pathogenesis of BA.
The down regulation of TRIF (zeige TRIM69 Antikörper), TLR3, and mitochondrial antiviral signaling protein (MAVS (zeige MAVS Antikörper)) expressions in chronic hepatitis C correlates with the disease severity and the outcome of hepatitis C virus infection
this study shows that Tlr3 in nasal CD103 (zeige ITGAE Antikörper)(+) 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 Antikörper) pathway inhibits polyposis through suppression of c-Myc (zeige MYC Antikörper) expression and supports long survival in Apc (zeige APC Antikörper) (Min/+) mice.
PolyI:C targeted Toll-like receptor 3 with minimal effect on the mitochondrial antiviral-signaling protein (zeige MAVS Antikörper) 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 Antikörper) 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 (zeige HCFC2 Antikörper) is a critical component of the IRF1 (zeige IRF1 Antikörper) and IRF2 (zeige IRF2 Antikörper) transcriptional machinery that regulates Tlr3 gene expression.
the JAK (zeige JAK3 Antikörper)-STAT (zeige STAT1 Antikörper) 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 (zeige TLR7 Antikörper) pathways.
RIG-I (zeige DDX58 Antikörper) and TLR3 interact with the pseudoknot of Porcine Reproductive and Respiratory Syndrome Virus 3' untranslated regions. Both RIG-I (zeige DDX58 Antikörper) and TLR3 are required for the pseudoknot to induce interferon (zeige IFNA Antikörper) response.
These data demonstrated that TLR2, TLR3 and TLR9 (zeige TLR9 Antikörper) contribute to NF-kappaB (zeige NFKB1 Antikörper) activation in response to porcine epidemic diarrhea virus infection, but not RIG-I (zeige DDX58 Antikörper).
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 Antikörper) 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 Antikörper) and TLR8 (zeige TLR8 Antikörper) 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 Antikörper)-/- 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