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Validated All-in-One™ qPCR Primer for TLR7(NM_016562.3) Search again
Product ID:
HQP012591
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
IMD74, SLEB17, TLR7-like
Gene Description:
toll like receptor 7
Target Gene Accession:
NM_016562.3(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 predominantly expressed in lung, placenta, and spleen, and lies in close proximity to another family member, TLR8, on chromosome X.
Gene References into function
- Human TLR7 or TLR8 independently confer responsiveness to the antiviral compound R-848.
- Interferon-alpha and interleukin-12 are induced differentially by Toll-like receptor 7 ligands in human blood dendritic cell subsets.
- IRF5 and IRF7 are critical mediators of TLR7 signaling
- Plasmacytoid dendritic cell-derived type I IFN enhanced TLR7 sensitivity of B cells by selectively up-regulating TLR7 expression
- TLR7 acts as a host sensor for human parechovirus 1, and activates signalling that leads to the synthesis of pro-inflammatory molecules by the host.
- The agonist isatoribine resulted in dose-dependent changes in immunologic biomarkers and a statistically significant antiviral effect with relatively few and mild side effects in hepatitis C.
- TLR9 may have a critical role in the promotion of lupus through the induction of IFN-alpha by predendritic cells.
- evidence showing that a ligand of Toll-like receptor 7 (TLR7) can induce anti-HCV immunity not only by IFN induction, but also through an IFN-independent mechanism
- TLR-7 "licenses" human B cells to respond to cytokines of the adaptive immune system (such as IL-2) and provide a strategy to increase the immunogenicity of lymphoma cells for therapeutic purposes
- Stimulation of in vitro-generated murine Toll-like receptor 7 (TLR7) knockout DC and human TLR-transfected HEK293 cells with dsRNA fragments gave no evidences for the involvement of pDC-specific TLR7 or TLR9 in the observed IFN-alpha induction.
- A profound sex-dependent pathway of TLR7-induced interferon (IFN)-alpha production is revealed with higher production in females.
- 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
- Autoantibody production is largely dependent on Toll-like receptor 7 (TLR7) and causes kidney pathology in nucleic acid-containing autoantigen knockin mice.
- These data lead us to suggest that ongoing viral activation of TLR7/8 could alter the adaptive immune response by modifying DC differentiation and by down-regulating DC responsiveness to a subsequent bacterial TLR4-mediated signal.
- TLR8 inhibits TLR7 and TLR9, and TLR9 inhibits TLR7 but not vice versa in HEK293 cells transfected with TLRs in a pairwise combination.
- results implicate involvement of toll-like receptors, particularly TLR7, and type 1 specific interferon signaling in the pathogenesis of BA, especially in early stage, which is associated with upregulation of inflammatory cytokines IL-8
- Our data reveal for the first time a strong inhibitory effect of TLR7 stimulation on IFN-alpha production induced by CpG-A- and CpG-C-ODNs.
- The c.1-120G TLR7 allele offers protection from the development of inflammation and fibrosis in male patients with chronic HCV-infection.
- CYLD, a novel deubiquitinase, acts as a negative regulator of TLR7 induction by nontypeable Haemophilus influenzae
- Epstein-Barr virus initially uses TLR7 signaling to enhance B-cell proliferation and subsequently modifies the pathway to regulate IRF-5 activity.
- Both types of compounds induced IFN-gamma-inducible protein 10, but only the 7-deazaguanosine-containing compound that activated both TLR7 and TLR8 induced IFN-alpha in monkeys
- relative gene copy number of TLR7 was not significantly increased among our SLE patients as compared with our controls.No trend between the relative gene copy number and the autoantibody profile in SLE patients.
- IFN-alpha produced after HIV-induced TLR7 stimulation was responsible for TRAIL expression and the down-regulation of both CXCR4 and CCR5 by IKpDC
- 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.
- This study reports the association of TLR7 variants with chronic HCV-infection and with the response to interferon-alpha therapy in patients with chronic HCV-infection.
- Direct involvement of human TLR7 is demonstrated in the induction of tumor necrosis factor (TNF)-alpha by single-stranded RNAs in the macrophage-like THP-1 cell line.
- TLR variants are unlikely to have a major impact on overall AMD risk, and the common variants studied were not associated with AMD.
- 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]
- These results delineate the complex effects of triggering TLR7/8 for an efficient antiviral defense.
- TLR-7 signaling stimulates apoptosis resistance, associated with enhanced iNOS expression (protein and mRNA) and NO release, notably through an NF-kappaB-dependent activation of the NO pathway.
- 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
- the Toll-like receptor 7 agonist imiquimod inhibits melanogenesis and proliferation of human melanocytes
- replicated association was obtained for SNPs or haplotypes of TLR7 and TLR8, suggesting these genes as novel disease genes for asthma and related disorders.
- Divergent TLR7 and TLR9 signaling and type I interferon production distinguish pathogenic and nonpathogenic AIDS virus infections.
- Up-regulation of natural killer cell function against head and neck cancer in response to single-stranded immunostimulatory RNA requires TLR7.
- Perturbation of TLR-7 on naive human B cells can lead to the induction of immunoglobulin class switch and IgG production in the absence of B-cell receptor cross-linking and CD40-CD40L interaction.