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Validated All-in-One™ qPCR Primer for TLR9(NM_017442.3) Search again
Product ID:
HQP104821
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
CD289
Gene Description:
toll like receptor 9
Target Gene Accession:
NM_017442.3(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 gene is preferentially expressed in immune cell rich tissues, such as spleen, lymph node, bone marrow and peripheral blood leukocytes. Studies in mice and human indicate that this receptor mediates cellular response to unmethylated CpG dinucleotides in bacterial DNA to mount an innate immune response. [provided by RefSeq].
Gene References into function
- TLR9 acts at the cell surface and engages an intracellular signaling pathway that includes MyD88, IRAK, and TRAF6
- Toll-like receptor 9 functions in the activation of RF expressing B-cells.
- In naive B cells, the expression of TLR9 and TLR10 is rapidly induced following B-cell-receptor (BCR) triggering. In contrast, memory B cells express several TLRs at constitutively high levels.
- All nine patients expressed all of the TLRs studied, whereas only five out of the nine patients had any granulomas positive for IL-4.The associations between TLRs 1, 5, and 9 were different in IL-4-negative compared with IL-4-positive patients.
- normal and neoplastic human B lymphocytes express a distinct TLR repertoire including TLR9 and TLR10 and expression is increased upon engagement of the antigen receptor complex or TLR9 itself
- Costimulation with TLR9 (or TLR2) and TLR4 induces synergistic release of Th1 cytokines, IFN-gamma and TNF-alpha, and additive HIV-LTR trans-activation and HIV replication, as measured by p24 antigen release from HIV-1 transgenic mouse spleen cells.
- A synergistic role is played by the TLR9/CD40 system in the orchestration of CpG-ODN-induced responses in B lymphocytes.
- peptidoglycan signaling through TLR2 and bacterial CpG DNA signaling through TLR9 are functionally equivalent at synergizing with IFN-gamma in regulating Tap-1 expression in macrophages
- mechanism of cellular activation involving the recruitment of TLR9 from the ER to sites of CpG DNA uptake, where signal transduction is initiated
- TLR signals that activate NF-kappaB are diverse among different TLRs, and TLR9 signaling uniquely depends on IRF-8 in DCs.
- mechanism of TLR9 gene regulation
- Toll-like receptor 9 binds single-stranded CpG-DNA in a sequence- and pH-dependent manner.
- TLR9 expression may function as a proinflammatory activation marker during the transition from monocyte to dendritic cells.
- Moreover, the TLR9 transfectant demonstrated its usefulness for evaluation of immunostimulation by bacterial DNA through the detection of T(H)-1, T(H)-2 type cytokine induction via TLR9 signaling.
- The expression of functionally active TLR9 in human malignant tumors might affect treatment approaches using CpG-ODN and shows that malignant cells can be regarded as active players in tumor-immunology.
- TLR9 gene polymorphisms were not significantly associated with the susceptibility to systemic lupus erythematosus in Korean patients.
- The TLR9 was analyzed by ICS as it was reported to be expressed in an intracellular compartment.
- a CpR dinucleotide is recognized by TLR9 and leads immune-cell activation and cytokine secretion in vitro and in vivo
- Diminished expression and function of TLR9 is a likely consequence of chronic filarial antigen stimulation and could serve as a novel mechanism underlying the dysfunctional immune response in lymphatic filariasis
- results demonstrated that TLR9 expression is correlated with immune activation and differs between individuals with non-activated or chronically immune activated background
- Data indicate that the two TLR-9 promotor polymorphisms are not involved in atherogenesis.
- TLR9 may have a critical role in the promotion of lupus through the induction of IFN-alpha by predendritic cells.
- TLR9- and FcepsilonRI-mediated responses oppose one another in plasmacytoid dendritic cells by down-regulating receptor expression.
- Activation of TLR-9 induces IL-8 secretion through peroxynitrite signaling in neutrophils.
- Broad TLR9 activation defects in common variable immune deficiency prevent CpG-DNA-initiated innate immune responses; these defects may lead to impaired responses of plasmacytoid dendritic cells and loss of B cell function.
- Bacterial DNA preparations from different species differ in their capacity to activate TLR-9, which is dependent on the individual [CG] content. Moreover, increased intracellular delivery results in a marked enhancement of immunostimulation.
- significant increase of the combined carriership of the CD14 -260T and TLR9 -1237C alleles in the chronic relapsing pouchitis group suggests that these markers identify a subgroup of patients with a risk of developing chronic or refractory pouchitis
- we here demonstrate that S. pneumoniae, H. influenzae, and N. meningitidis each activate several TLRs in species-specific patterns and show that infection with live pathogens may lead to activation of PRR not targeted by inactivated bacteria.
- TLR4 and TLR9 polymorphisms increased the risk of low birth weight in infants; polymorphisms of TLR4 increased the risk of maternal anemia.
- 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
- Toll-like receptor 9 (TLR9) recognizes microbial DNA. We show here that TLR9 protein is expressed in human breast cancer cells and clinical breast cancer samples.
- This establishes that the primary determinant of TLR9 signaling is not valency but endosomal location and demonstrates a strict compartmentalization of the biological response to TLR9 activation in plasmacytoid dendritic cells (PDCs).
- Plays a role of in the recognition of M. bovis BCG by dendritic cells.
- TLR2 and TLR9 cooperate in the control of parasite replication during Trypanosoma cruzi infection; TLR9 has a primary role in the MyD88-dependent induction of IL-12/IFN-gamma synthesis during infection with T. cruzi.
- The results of this study suggest a model where modification of the cytoplasmic tail of TLR9 results in trafficking to early endosomes where it encounters CpG DNA.
- reviews experience with two distinct therapeutic strategies: TLR9-based immunomodulation and TLR9-based vaccination
- TLR8 inhibits TLR7 and TLR9, and TLR9 inhibits TLR7 but not vice versa in HEK293 cells transfected with TLRs in a pairwise combination.
- In patients with active systemic lupus erythematosus, the proportion of peripheral blood memory B cells and plasma cells expressing TLR-9 is increased
- HMGB1 suppresses PDC cytokine secretion and maturation in response to TLR9 agonists including the hypomethylated oligodeoxynucleotide CpG- and DNA-containing viruses
- immune cells use several mechanisms to discriminate between stimulatory and nonstimulatory DNA; however, it appears that TLR9 itself binds rather indiscriminately to a broad range of DNAs
- Development of skin lesions in mycosis fungoides appears associated with an increase of TLR9 expression by keratinocytes in cutaneous lesions.
- 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
- Human peripheral blood B cells express TLR9 and that its expression is increased in patients with Systemic Lupus Erythematosus.
- Rapid progression of HIV-1 infection was associated with TLR9 polymorphisms
- These results demonstrate that intestinal epithelial cells recognize pathogenic bacterial DNA and respond by increasing surface localization and expression of TLR9.
- The widespread expression of TLR9 in the nasal mucosa along with its rich representation in leukocytes in different compartments.
- The presence of the G allele at position +1174 of TLR9 predisposes humans to an increased risk of SLE.
- TLR9-mediated invasion may represent a novel mechanism through which infections promote prostate cancer.
- TLR9 expression, which was mainly observed as cytoplasmic staining, gradually increased in accordance with the histopathological grade
- These findings suggest that tubular TLR-9 activation has a pathogenetic role in tubulointerstitial inflammation and damage in experimental and human lupus nephritis.
- TLR-9 may play a role in the regulation of the hypothalamic-pituitary-adrenal axis during conditions in which bacterial DNA is present.
- Our results do not indicate a major influence of these putative functional TLR5 and TLR9 single nucleotide polymorphisms on the susceptibility to (or protection from) systemic lupus erythematosus.
- TLR 9 play a distinct role in the inflammatory response that clears viruses from the retina.
- the TLR9 promoter polymorphism C-1237T might affect atopic eczema susceptibility in particular in patients with the intrinsic variant of AE
- synthetic agonists of TLR9 interfere with growth and angiogenesis also by epidermal growth factor receptor- and antibody-dependent cell-mediated cytotoxicity-independent mechanisms affecting endothelial cell functions
- Overexpression of TLR9 is associated with B-chronic lymphocytic leukemia
- SNPs in the TLR9 gene were not significantly associated with susceptibility to Behcet's disease
- Patients with severe and mild malaria showed increased surface expression of TLR2 and TLR4 on CD14(+)monocytes and myeloid dendritic cells and decreased intracellular expression of TLR9 on plasmacytoid dendritic cells compared to healthy controls.
- suggest the existence of an IRAK-4-independent TLR9-induced transduction pathway leading to PI3K activation
- direct CpG-oligodeoxynucleotides and TLR-9 interactions in HT-29 cells could provide new approaches in malignant tumor therapeutic strategies
- polymorphism of TLR9 gene is significantly associated patients with mold infections, suggesting a possible role for this genetic variant as a risk factor for mold infections in pediatric patients receiving chemotherapy for hematological diseases
- TLR9 variants were not major risk factors for Crohn's disease in New Zealand population, but may associations with disease worldwide.
- Btk as a key signaling molecule that interacts with and acts downstream of TLR8 and TLR9.
- an NF-kappaB luciferase reporter assay in human embryonic kidney cells transfected with human TLR9 demonstrated that Entamoeba histolytica DNA signaled through Toll-like receptor 9 (TLR9) in a manner similar to that seen with CpG-oligodeoxynucleotides.
- Functional expression of TLR9 is associated to the metastatic potential of human lung cancer cell.
- Autocrine TNF-alpha secretion resulting from IgE/FcepsilonRI-dependent activation plays a critical role in suppressing TLR9-dependent responses in plasmacytoid dendritic cells that normally promote T(H)1 activity
- Benign prostate epithelial cells express both TLR 4 (LPS-specific) and TLR 9 (CpG-specific) when exposured to lipopolysaccharide (LPS) and CpG DNA.
- abnormality of innate immunity plays a crucial role in the pathology of sysemic lupus erythematosus: blockade of CpG-TLR9 interaction may be a new therapeutic approach.
- no significant association with multiple sclerosis and no protective effect of T-1237C concerning age of onset, disease severity or disease subtype in patients
- expression of TLR9 within human glioblastomas strengthens the rationale for the utilization of oligonucleotides containing CpG motifs in this disease
- This review will focus on the roles of TLR9 in immune responses, and its signaling pathways--REVIEW
- Susceptibility to allergic bronchopulmonary aspergillosis was associated with allele C on T-1237C (Toll like receptor 9)
- it was concluded that TLR9 and CD14 gene polymorphisms may contribute to an inherited predisposition to asthma in Tunisian children.
- Impaired TLR9-dependent immune responses in Human plasmacytoid dendritic cells (pDCs) are associated with allergic status and inversely correlated with Fc epsilon RI alpha expression.
- these data demonstrate that TLR9 detects A. fumigatus DNA, resulting in the secretion of proinflammatory cytokines, which may contribute to the immune response to the pathogen.
- TLR7-9 recognize single-stranded RNA, nucleoside analogs and single-stranded CpG-DNA, respectively, and their activation initiates the immune response against viruses and bacteria [review]
- 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
- B cells from HIV-infected persons express reduced levels of TLR9 mRNA, and this defect is especially pronounced among memory B cells
- CD300a and CD300c play an important role in the cross-regulation of TNF-alpha and IFN-alpha secretion from pDCs; CD300a/c RNA and surface expression were downregulated after stimulation of pDCs with TLR7 and TLR9 ligands
- Targeting toll-like receptor 9 with CpG oligodeoxynucleotides enhances anti-tumor responses of peripheral blood mononuclear cells from human lung cancer patients.
- study demonstrated that infection with Trypanosoma cruzi parasites promotes recruitment of TLR9 to the endo-lysosome compartment
- TLR9 is expressed in idiopathic interstitial pneumonia and its activation promotes in vitro myofibroblast differentiation.
- activation of the TLR9/MyD88 pathway by common antigens may affect the severity of IgAN
- Divergent TLR7 and TLR9 signaling and type I interferon production distinguish pathogenic and nonpathogenic AIDS virus infections.
- Activation of human plasmacytoid dendritic cells by TLR9 impairs Fc gammaRII-mediated uptake of immune complexes and presentation by MHC class II
- TLR9 expression is increased in breast cancer and CpG oligonucleotide-induced cellular invasion is mediated via TLR9 and TRAF6, independent of MyD88.
- Toll-like receptor 2, 4, and 9 overexpression is associated with neutrophil dysfunction in alcoholic hepatitis.
- TLR9-mediated B cell stimulation induces zeta-chain associated protein kinase 70kDa (ZAP70) expression; ZAP70 expression in human B cells represents an exclusive hallmark of TLR9-mediated B cell activation.
- Stimulation of innate immunity via toll-like receptor 9 is highly effective at reducing the parenchymal and vascular amyloid burden in an animal model of Alzheimer's disease.