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Validated All-in-One™ qPCR Primer for TLR3(NM_003265.2) Search again
Product ID:
HQP018115
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
CD283, IIAE2, IMD83
Gene Description:
toll like receptor 3
Target Gene Accession:
NM_003265.2(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
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| A | B |
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Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
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Summary
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. [provided by RefSeq].
Gene References into function
- the first demonstration of the importance of TLR3 cytoplasmic tyrosine residues in double-stranded RNA signaling
- TLR3 has a role in innate and adaptive immune responses
- TLR4-mediated activation of the interferon-sensitive response element has an absolute requirement for NFKBp65, whereas the TLR3-induced ISRE response is NFKB-independent
- measles virus-induced expression of TLR3 may reflect amplified IFN production that plays a part in host defense to viral infection
- RNA, likely through secondary structure, is a potent host-derived activator of TLR3
- double-stranded RNA-induced TLR3/TRIF-mediated NF-kappaB and IRF3 activation diverge at TRIF
- This isoform has 2,520 bp cDNAs compared to the 2,712 bp of full cDNA, is produced by deletion of an intron-like sequence within exon 4 and is co-expressed with wild type TLR3 in primary human astrocytes and glioblastoma cell lines.
- siRNA and shRNA knockdown of genes represents a new and powerful tool, it is not without nonspecific effects, which we demonstrate are mediated in part by signaling through TLR3.
- Data support the hypothesis that toll-like receptor-3 is an important determinant of cellular responses to external double-stranded RNA.
- the cytoplasmic linker region of TLR3 regulates receptor retention inside the organelle and signaling
- With expression of TLR3, poly I:C stimulation induces the activation of interferon regulatory factor-3.
- dsRNA-activated phosphorylation of two specific tyrosine residues of TLR3 is essential for initiating two distinct signaling pathways
- TLR3 is constitutively expressed in human alveolar and bronchial epithelial cells; TLR3 contributes directly to the immune response of respiratory epithelial cells to influenza A virus and dsRNA
- Resting and activated human astrocytes preferentially express TLR3, constitutively express adapters linked to TLR3 signaling, and respond to TLR3 engagement with production of TNF-alpha, IL-6, and chemokines.
- studies indicate that TLR3 mediates inflammatory cytokine and chemokine production in respiratory syncytial virus-infected epithelial cells.
- hepatocytes contain two distinct antiviral signaling pathways leading to expression of intereron beta, one dependent upon TLR3 and the other dependent on RIG-I, with little cross-talk between these pathways
- Toll-like receptor 3, although essential for gene induction by dsRNA, was dispensable for gene induction by Sendai virus
- IFN-alpha-induced up-regulation of TLR3 expression is involved in dsRNA activated antiviral response in human epithelial and endothelial cells
- The gene expression and surface expression of TLR3 in polyI:C-stimulated corneal epithelial cells.
- TLR3 is involved in the immune responses of endometrial epithelial cells after exposure to dsRNA and has the potential to alter the cytokine milieu and influence the outcome and consequences of infection.
- crystal structure of ectodomain; large horseshoe-shaped solenoid assembled from 23 leucine-rich repeats (LRRs)
- TLR3 and TLR4 signal primarily through NF-kappaB to enhance transcription of pIgR mRNA.
- These results suggest that polymorphisms in the TLR3 gene, which is part of the innate immune system, may be associated with type 1 diabetes in this population.
- Biliary epithelial cell antibodies via induction of TLR2 and TLR3, as well as inflammatory cytokine and chemokine production may induce epithelial cell inflammatory responses to bacterial components and contribute to posttransplantation cholangitis.
- The overall horseshoe-shaped structure of the TLR3-ectodomain is formed by 23 repeating leucine-rich repeats (LRRs) that are capped at each end by specialized non-LRR domains.
- TLR3 engagement by poly(I-C) at an acidic pH, probably in early phagolysosomes or endosomes, induces receptor aggregation leading to signaling
- The up-regulation of Toll-like receptors 2, 3 and 4 in the nasal mucosa of patients with symptomatic allergic rhinitis supports the idea of a role for Toll-like receptors in allergic airway inflammation.
- This study demonstrates an important functional requirement for TLR3 in the host response against rhinovirus infection
- required for the activation of NFkappaB by the LTRf from Moloney murine and feline leukemia viruses
- The role of TLR3 in the immunobiology of muscle is reported; its implications for the understanding of the pathogenesis of inflammatory myopathies or therapeutic interventions are included.
- Exposure of respiratory epithelial cells to diesel exhause enhances virus and could potentially alter the response to viral infections by increasing the expression and function of TLR3.
- Respiratory syncytial virus, via an effect on TLR3 and protein kinase R, sensitizes airway epithelial cells to subsequent double-stranded (ds)RNA exposure.
- TLR3 is induced on human astrocytes upon inflammation and when activated, mediates a comprehensive neuroprotective response rather than a polarized pro-inflammatory reaction.
- the interaction of IRF-8 with TRAF6 modulates TLR signaling and may contribute to the cross-talk between IFN-gamma and TLR signal pathways
- analysis of glycosylation of human Toll-like receptor 3
- direct proapoptotic activity of endogenous TLR3 expressed by cancerous cells
- the STAT1-SOCS1 pathway regulates the innate immune response via TLR3 signaling in epidermal keratinocytes
- These mutations locate the dsRNA binding site on the glycan-free, lateral surface of TLR3 toward the C terminus and suggest a model for dsRNA binding and TLR3 activation.
- findings demonstrate that TLR-3 and TLR-9 mediate the activation of corneal cells by Herpes simplex virus 1, HSV-1 DNA and HSV-1-antibody complexes
- TLR3 associates with activated c-Src tyrosine kinase double-stranded (ds)RNA-containing endosomes in HeLa cells, and triggers an innate immune response during viral infection.
- brain neurons can express TLR-3 in vivo and these neurons may play an important role in initiating an inflammatory reaction in a variety of neurological diseases
- H. influenzae infection increases airway epithelial cell ICAM-1 and TLR3 expression, leading to enhanced binding of RV and a potentiation of RV-induced chemokine release
- TLR3 agonist poly(I:C) activated epithelial cells, primary endothelial cells, and two types of primary human smooth muscle cells (airway [ASMC] and vascular) directly, while the TLR7/8 agonist R848 required the presence of leukocytes to activate ASMC
- Evidence of a functional response to TLR ligand TLR3 supports an immunomodulatory role for airway smoooth muscle cells during airway inflammatory responses.
- TLR3-mediated production of proinflammatory cytokines and chemokines in oviduct epithelial cells in response to viral dsRNA may be important for antiviral immunity in the human female reproductive tract.
- Human neurons express TLR-3, a major receptor in virus-mediated innate immune response.
- Both the cytoplasmic and TLR3-mediated dsRNA recognition pathways converge upon NAP1 for the activation of the IRF-3 and IFN-beta promoter.
- TLR3 ligands can not only indirectly influence the adaptive immune response through modulation of dendritic cell activation, but also directly increase IFN-gamma production by Ag-specific CD8+ T cells.
- The interactions between the TLR3 ectodomain and double-stranded RNA depended on acidic pH.
- Two phosphotyrosine residues of Toll-like receptor 3 (TLR3) activate two distinct pathways, one leading to NF-kappaB release and the other leading to its phosphorylation.
- dimer of TLR3 is the form that binds RNA and activates signal transduction.
- A molecular model of TLR# in order to understand the molecular basis of pathogen associated molecular patterns.
- expression levels of TLR2, TLR3, TLR4 & TLR9 in endometrium varied in a similar pattern during the menstrual cycle; levels were high in perimenstrual period & low in periovulatory period
- Results suggest that N284I and L412F affect the activities of Toll-like receptor 3 needed for proper signaling.
- TLR3, PI3K, and IRF3 are involved in the poly IC-induced galectin-9 expression in HUVECs
- These results suggest that the extracellular domains are a crucial trigger of cytoplasmic interferon signaling in TLR3.
- Ability of phenylmethimazole (C10) to decrease growth and migration of papillary thyroid cancer cells may be related to its suppressive effect on TLR3 and Wnt5a signaling.
- TLR 3 play a distinct role in the inflammatory response that clears viruses from the retina.
- TLR3 is able to sense both single-stranded RNA and dsRNA
- Flow cytometry showed that the nasal polyp epithelial cell mainly expressed TLR3 in an intracellular compartment; immune response of these cells induced by TLR3 could not be blocked by anti-TLR3 antibody.
- poly(I:C) upregulated TLR3, thereby augmenting the primary (IFN-beta) and secondary (IDO and viperin) response genes
- Cell type- and species-specific response for TLR stimulation.
- TLR3 is predominantly expressed on the cell surface of native natural killer cells and becomes rapidly internalized in response to the head and neck squamous cell carcinoma microenvironment.
- Activation of human microglia via Toll-like receptors, particularly TLR3, can change profile of local central nervous system immune responses by translating Th1 polarizing signals to CD4 T cells.
- Viral dsRNA recognition by TLR3 expressed in airway smooth muscle cells may contribute to airway hyperreactivity by differentially regulating M2R and M3R expression and function.
- study reports a dominant-negative TLR3 allele in otherwise healthy children with herpes simplex virus 1 encephalitis; TLR3 appears to be redundant in host defense to most microbes but is vital for natural immunity to HSV-1 in the CNS
- TLR3 is overexpressed in clear cell renal cell carcinoma
- TLR3 polymorphisms may be relevant to nasopharyngeal carcinoma susceptibility in the Cantonese population.
- Our data suggest that the intestinal microvasculature is responsive to ligands of TLR3 expressed on intestinal endothelial cells, thereby adding to the regulation of adaptive immunity and leukocyte recruitment.
- findings show that NK cells display heterogeneous levels of TLR3 mRNA transcript; clones displaying higher TLR3 mRNA transcripts were characterized by higher cytokine production and cytotoxicity
- TLR3 expression on mesenchymal stem cells (MSCs) may provide an effective mechanism to block the immunosuppressive activity of MSCs and therefore to restore an efficient T-cell response in the course of dangerous infections
- the spatiotemporal mobilization of TICAM-1 in response to dsRNA and the formation of the TICAM-1 speckles containing RIP1 and NAP1 are important for the activation of the TLR3-TICAM-1 pathway.
- Our results show that PAMP receptors, TLR3, TLR7 and RIG-I mRNA levels are significantly down-regulated in patients with chronic hepatitis C infection when compared with healthy controls.
- Mutagenesis approach showed that conserved histidine residues were essential for the ligand-dependent activation of TLR3.
- TLR3 assembles on dsRNA as stable dimers and the minimal signaling unit is one TLR3 dimer
- These data suggest that TLR3 contributes to the malignant phenotype leading to invasive carcinoma in head and neck squamous cell carcinoma.
- Data report that dendritic cell stimulation through the Toll-like receptor 3 ligand dsRNA [poly(I:C)] limits CD4 T-cell proliferation, curtailing adaptive immune responses.
- we summarize the current knowledge on TLR3 and discuss its possible role in innate and adaptive immunity--REVIEW
- Small interfering RNAs directed against TLR3 greatly reduced the ability of Kaposi's sarcoma-associated herpesvirus to upregulate IFN-beta1 and CXCL10 upon infection
- TLR variants are unlikely to have a major impact on overall AMD risk, and the common variants studied were not associated with AMD.
- TLR3 and 9 as well as IFN-beta and TNF-alpha are expressed in verruca and molluscum contagiosum skin lesions and may play a pivotal role in cutaneous innate immune responses
- cytomegalovirus M45 protein provides a direct cell type-dependent replication benefit to the virus while modulating other biological processes signaling via the RIP1 adaptor such as activation of Toll-like receptor (TLR)3 and other mediators of cell deat
- Binding of the glycosylated West Nile virus envelope protein DC-SIGN leads to a reduction in the expression of Toll-like receptor 3 (TLR3) in macrophages from young donors via the signal transducer and activator of transcription 1-mediated pathway.
- microfilariae interfere with monocyte-derived DC function by altering TLR3 and TLR4 expression and interfering with both MyD88-dependent signaling and a pathway that ultimately diminishes NF-kappaB activity
- Novel model for the formation of TLR3 ectodomain dimers complexed with double strnded RNA, which incorporates this second binding site.
- West Nile virus nonstructural protein 1 inhibits TLR3 signal transduction.
- Prostate cancer cell lines express TLR3 and the TLR3 agonist poly (I:C) activates mitogen-activated protein kinases and induces inhibition of proliferation as well as caspase-dependent apoptosis.
- viral dsRNA may initiate frontline IgG and IgA responses through an innate TLR3-dependent pathway involving BAFF
- There are different arrangements of TLR3 ectodomains along the double-stranded RNA that could modulate the strength of the interferon response.
- TLR3 double-stranded DNA sensing receptor is a dominant stimulator of antiviral pattern recognition molecules and NF-kappaB-induced gene activation in human keratinocytes.
- caspase-8 has a role in the production of biologically active IL-1beta in response to TLR3 and TLR4 stimulation
- The TLR3 412Phe variant confers protection against geographic atrophy in macular degeneration.
- Our data suggest an involvement of TLR3 and TLR4 in endometrial diseases as demonstrated by altered expression levels in endometriosis and endometrial cancer.
- These results suggest that p53 influences TLR3 expression and function and highlight a role of p53 in innate immune response in epithelial cells.
- dsRNA is recognized by differently categorized receptors, cytoplasmic RIG-I-like receptor, membrane-bound TLR3 and cell-surface RNA capture. The endocytic pathway is critical for dsRNA-induced TLR3-mediated cell activation.
- TLR3 has a major role in the development of ARDS-like pathology in the absence of a viral pathogen.
- Results indicate that TLR3 expression in hepatocellular carcinoma plays an important role with regard to cell survival and proapoptotic activity.
- Toll-like receptors 3 highly expressed on human melanoma cells.
- high expression of TLRs 3 and 4, at an early stage of rheumatoid arthritis and the reactivity of synovial fibroblasts in vitro suggest that TLR signaling pathways resulting in inflammation and joint destruction are activated early in the disease process
- These results suggest that through DC activation, human TSLP and TLR3 ligands promote differentiation of Th17 cells with the central memory T cell phenotype under Th2-polarizing conditions.