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Human TLR9 Protein expressed in Wheat germ - ABIN1330558
Julian, Shao, Vangundy, Papenfuss, Crouser: Mitochondrial transcription factor A, an endogenous danger signal, promotes TNF? release via RAGE- and TLR9-responsive plasmacytoid dendritic cells. in PLoS ONE 2013
There is a relationship between sepsis-induced immunosuppression and serum TLR-9 levels. The host immunity system can be activated by means of TLR-9-related systems, while hyperlactatemia may play a stimulating role in the re-activation of the immune system.
TLR9 is capable of robustly suppressing angiogenesis by differentially regulating the expression of VEGFA and sFLT1 at the fetomaternal interface, potentially contributing to the development of Preeclampsia.
rs187084 AA genotype of TLR9 is associated with Hepatitis B virus progression to advanced liver disease
SNPs in TLR8 and TLR9 were associated with the development of tuberculosis; those SNPs may have different effects on disease pathogenesis and progression.
This study provides evidence that TLR9 affects human S. aureus immunity and present potential explanations for differences according to sex in S. aureus colonization and infection.
decrease in full-length protein levels in substantia nigra of Parkinson disease patients
The authors showed that dendritic cell treatment with a TLR9 agonist results in an increase in fungicidal activity of these cells against the fungus Paracoccidioides brasiliensis.
TLR9 activation is augmented by short single-stranded DNA degradation products
The detection of higher frequencies of the TLR2, TLR4 and/or TLR9 polymorphisms in colorectal cancer (CRC) patients compared with the control groups highlight the role of these polymorphism in CRC development and cancer progression
TLR4 and TLR9 mRNA were elevated in blood samples from celiac disease patients compared to the healthy controls
Finding suggest that genetic variations in TLR9 (rs352139 and rs352140) are associated with severity and prognosis of bacterial meningitis in Chinese children.
The findings show that the expression of TLR2, TLR4 and TLR9, and hypoxia markers HIF-1alpha and CAIX is abnormal in pancreatic intraepithelial neoplasia suggesting that both the innate immunity activation and hypoxia response are involved in early pancreatic carcinogenesis.
Genotyping was performed to detect -T1237C (rs5743836) and G2848A (rs352140) SNP in TLR9 gene in patients with pulmonary tuberculosis and healthy controls. The A allele of G2848A SNP in TLR9 gene was found with a marginally higher frequency among tuberculosis patients.
The TLR3.rs3775290 "CC" genotype was associated with hepatitis C virus chronicity, while the TLR9 gene may not play a major role in hepatitis C virus infection.
Identify both expansion of T-bet(+) B cells and production of anti-erythrocyte antibodies in ex vivo cultures of naive peripheral blood mononuclear cells exposed to P. falciprum infected erythrocyte lysates. We propose that synergistic TLR9/IFN-gammaR activation of T-bet(+) B cells is a mechanism underlying infection-induced autoimmune-like responses.
TLR9, especially TLR9/CD3, is highly expressed in systemic sclerosis patients particularly those with diffuse cutaneous subtype and could form a potential marker for skin fibrosis and disease severity.
TLR9 Gene Polymorphism is not associated with Chronic Lymphocytic Leukemia.
TLR-9 gene rs187084 polymorphism is positively correlated with susceptibility to Osteoarthritis of Knee, especially among old people in a Chinese population.
Data showed strong interactions of toll-like receptors TLR2 and 4 associated with Leishmania(V.) braziliensis, while toll-like receptor TLR9, in contrast, a strong interaction with Leishmania (L.) amazonensis.
Studied associations of 12 single nucleotide polymorphisms (SNPs) within toll like receptor genes (TLR2, TLR3, TLR4, and TLR9) and genetic predisposition to newborn severe hepatitis.
High TLR9 expression causes inflammatory myopathy.
These data indicate that sepsis-induced cardiac dysfunction requires presence of TLR3 and TLR9 and may be linked to histone-induced damage of cardiomyocytes.
resulting in maturation-specific stabilization of TLR9 within endolysosomes and subsequent pro-inflammatory signaling
data thus indicates that EBV DNA itself acts as a modulator of the Th17 compartment as well as that of regulatory T cell mechanisms. The involvement of TLR9 in the EBV DNA-triggered induction of IL-17A.
Microglial glucocorticoid receptors regulate TLR9 trafficking and lysosomal environment. Loss of glucocorticoid receptors enables activation of a microglial TLR9 inflammatory pathway, which can play a role in the progression of Parksinson disease.
Study shows that placental and/or fetal DNA stimulates toll-like receptor 9 (TLR9) leading to secretion of pro-inflammatory cytokines by macrophage cells.
Plasmodium DNA induces autoreactive responses against erythrocytes by activating a population of B cells expressing CD11c and the transcription factor T-bet, which become major producers of autoantibodies that promote malarial anaemia.
Our findings suggested the collaboration of TLR2-TLR9 at least in the regulation of SARM expression.
High cholesterol intake exacerbated acetaminophen-induced acute liver injury via the accumulation of free cholesterol in the endolysosomes of liver sinusoidal endothelial cells. This accumulation enhanced Toll-like receptor 9 signaling via impairment of its membrane trafficking mechanism.
these data provide a previously uncharacterized in vivo mechanism contingent on oligodeoxy-nucleotide -administered dose, where TLR9 governs the primary response and RAGE plays a distinct and cooperative function in providing a pivotal role in balancing the immune response.
this study shows that CD205-TLR9-IL-12 axis contributes to CpG-induced oversensitive liver injury in Hepatitis B viral antigens transgenic mice by promoting the interaction of NKT cells with Kupffer cells
The findings support a salutary role of TLR9 in some subsets of HF conditions and underline the importance for future studies on the mechanisms of TLR9 in diastolic HF.
TLR9-driven inflammation induced a Ccr2-independent expansion of functionally enhanced extramedullary myeloid progenitors that correlated with the peripheral accumulation of monocytes in both wild-type and Ccr2(-/-) mice.
TLR9 expression on B1a cells is not critical for their IgM-dependent atheroprotection.
This study establishes a correlation between TLR-3 and TLR-9 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.
these data demonstrate that TLR7/TLR9 ligands push the macrophage into a phagocytic long-lived cell, with a decreased capacity of antigen presentation and reminiscent of the M2 polarized state.
TLR9/MyD88 signaling selectively in CD11c(+) dendritic cells (DCs) strongly enhances murine cytomegalovirus clearance.
Overall, the data reveal that the early recruited sTLR9(+) neutrophils may, at least in the area of local inflammation, play a protective role during SIRS development and provide a method to rescue the patients with severe SIRS via the up-regulation of sTLR9 levels on the surface of neutrophils or via adoptive therapy with protective sub-populations of neutrophils.
High-glucose induces tau hyperphosphorylation through activation of TLR9-P38 MAPK pathway.
these results indicate clear responses of porcine neonatal antigen presenting cells after TLR2 and TLR9 stimulation
Porcine parvovirus virus infection significantly induced IL-6 expression and this induction depended on NF-kappaB activation and TLR9 signaling pathways in PK-15 cell.
TLR9 immunoreactivity is mainly detected in epithelial cells and antigen presenting cells, namely dendritic and macrophage-like cells, within the range of tissues examined. The pattern of TLR9 expression was similar in pigs of 3 weeks and 3 months of age.
These data demonstrated that TLR2, TLR3 and TLR9 contribute to NF-kappaB activation in response to porcine epidemic diarrhea virus infection, but not RIG-I.
expression of TLR3, TLR7 and TLR9 in alveolar macrophages infected with different genotype 1 PRRSV strains
we studied TLR9 expression in lung extracts from pigs, dogs, and cattle.
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.
variants in the TLR1 gene are associated with susceptibility to bovine tuberculosis, whereas no significant association can be inferred from the polymorphisms in the TLR9 gene
mRNA abundances of TLR9, TLR2, and TLR4 together with those of beta-defensin 5 (BNBD5), an early bactericidal effector molecule of the innate system, in healthy and infected mammary glands
substantial conservation of TLR9 structure and TLR9 function in blood leukocytes
Comparative sequence analysis revealed a total of 139 polymorphisms, which include single-nucleotide polymorphisms and insertion-deletion polymorphisms.
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.
Toll-like receptor 9 protein