Goat Anti-Mouse CD289, N-terminus
- Known as:
- Goat Antibody toMouse CD289, N-terminus
- Catalog number:
- 129-10143
- Product Quantity:
- 100
- Category:
- -
- Supplier:
- Ray Biotech
- Gene target:
- Goat Anti-Mouse CD289 N-terminus
Related genes to: Goat Anti-Mouse CD289, N-terminus
- Gene:
- TLR9 NIH gene
- Name:
- toll like receptor 9
- Previous symbol:
- -
- Synonyms:
- CD289
- Chromosome:
- 3p21.2
- Locus Type:
- gene with protein product
- Date approved:
- 2001-04-27
- Date modifiied:
- 2016-10-05
Related products to: Goat Anti-Mouse CD289, N-terminus
Related articles to: Goat Anti-Mouse CD289, N-terminus
- Toll-like receptors (TLRs) play a significant role in the tumor microenvironment, including in brain tumors, as their activation can both support an anti-tumor response and promote tumor progression through chronic inflammation. However, the precise mechanisms of TLR action have not been fully elucidated, likely due to their complex role in both innate and adaptive immunity. The aim of this study was to analyze serum TLR2 and TLR9 concentrations in patients with glioma in the context of potential Epstein-Barr virus (EBV) infection. TLR9 levels were also analyzed in relation to the presence of viral DNA and EBER molecules in tumor tissue, as well as EBV-related serological responses. The results demonstrate that TLR2 and TLR9 levels were higher in patients with glioblastoma than in control groups. Notably, however, lower TLR9 concentrations were observed in patients testing positive for EBV. Furthermore, a detailed data analysis revealed a link between TLR9 levels and the presence of EBER molecules and/or EBV DNA in tumor tissue. Nevertheless, given the undefined role of EBV in the pathogenesis of glioblastoma, further intensive research in this area is required. - Source: PubMed
Publication date: 2026/09/21
Brzozowski MichałGóralczyk MagdalenaBogacki SylwesterPolz-Dacewicz Małgorzata - This study examined Toll-like receptors (TLRs)/chemokine receptors (CCRs) gene expression levels in HIV-infected individuals at different stages of HIV infection. It has been demonstrated that in the advanced stages of HIV infection, aggravated by () infection, there was a significant increase in , , , and expression levels (181-, 8.4-, 15-, and 3.4-fold, respectively), compared to the early stages of the disease, which also correlated with an increase in viral load. The advanced stages of HIV infection were also characterized by an increased expression level (8.08-fold, < 0.0001) on patients' mononuclear cells, which was not observed in the early stages of the disease. A positive correlation was found between the enhanced levels of / and expression, which facilitates the entry of HIV-1 into the cell (r = 0.03564, = 0.0423 for ; r = 0.3793, = 0.0269 for ). The advanced stages of HIV infection were characterized by a sharp increase in the expression levels of CXCR4 and CCR8 co-receptors which also play an important role in the entry of HIV-1 into the host cell (more than 537-fold, = 0.0006, and 5000-fold, = 0.004, respectively). At the advanced stages of HIV infection, a positive correlation was found between increased production of TLR and CCR and elevated expression of IL-12 and IL-18. These factors contribute to virus persistence and chronic immune activation observed in patients with opportunistic infections. Thus, the obtained data indicate that HIV-1 in the advanced stages of infection induces an increased TLRs and CCRs expression, which, together with enhanced viral production, leads to chronic inflammation and can contribute to tissue damage and exacerbate the disease's progression. - Source: PubMed
Publication date: 2026/09/14
Nosik MarinaBystritskaya ElizavetaRyzhov KonstantinKostyuchenko ElizavetaKuzina AnnaKravtchenko AlexeySevostyanihin SergeiDemenok IgorZverev VitalySvitich Oxana - is a Gram-negative opportunistic pathogen responsible for Legionnaires' disease, a severe form of atypical pneumonia associated with high morbidity and mortality, particularly in immunocompromised individuals. Despite its growing global burden and the persistence of environmental reservoirs, no licensed vaccine is currently available. In this study, an integrative immunoinformatics and reverse vaccinology approach was employed to design a multi-epitope vaccine candidate targeting . The complete proteome was systematically analyzed to identify essential, virulent, and surface-accessible proteins. Subsequent antigenicity assessment and non-homology screening against the human proteome led to the selection of key immunogenic targets, including KDO transferase and TolR. B-cell and T-cell epitopes were predicted and rigorously filtered based on antigenicity, non-allergenicity, and non-toxicity. Selected epitopes were assembled into a multi-epitope vaccine construct using appropriate linkers and adjuvants to enhance immunogenicity and structural stability. The designed construct exhibited favorable physicochemical properties, high antigenicity, and good solubility. Structural modeling and refinement confirmed the reliability of the predicted three-dimensional structure. Molecular docking analysis demonstrated strong binding interactions with immune receptors TLR-2 and TLR-9, which were further validated by molecular dynamics simulations indicating stable complex formation under physiological conditions. In addition, immune simulation predicted robust humoral and cellular immune responses, including memory cell generation. Overall, this study presents a promising computationally designed multi-epitope vaccine candidate against . However, further in vitro and in vivo studies are required to validate its immunogenicity, safety, and protective efficacy. - Source: PubMed
Publication date: 2026/09/08
Thangamani LokeshLian Tong - Preservation of mitochondrial integrity has emerged as a central hub in the anti-inflammatory effect of exercise. This narrative review advances a framework in which mitochondrial damage-associated molecular patterns (mtDAMPs) serve as the mechanistic bridge between exercise and inflammation. Mitochondrial dysfunction releases mtDAMPs, including mitochondrial DNA (mtDNA), reactive oxygen species, cardiolipin, N-formyl peptides, and ATP, which activate cGAS-STING, the NLRP3 inflammasome, TLR9, AIM2, ZBP1, and NF-κB signaling. Crosstalk among these pathways allows mild mitochondrial damage to escalate into chronic inflammation. Exercise opposes this cascade through the AMPK-PGC-1α axis, which coordinately activates four mitochondrial quality control (MQC) modules: biogenesis, antioxidant defense, dynamics, and mitophagy. The cardiovascular system illustrates this framework, as myocardial inflammation runs mainly through mtDNA-cGAS-STING signaling and vascular inflammation through oxidized mtDNA-NLRP3 signaling, while cardiovascular aging engages both axes at once. Throughout, exercise refers to repeated training rather than to a single bout, and the framework targets middle-aged and older adults with, or at risk of, cardiovascular disease. The upstream half of the sequence, in which training raises mitochondrial content and antioxidant capacity, rests on human muscle biopsy data; the downstream half remains largely preclinical. MQC is therefore proposed as a testable target rather than an established one. - Source: PubMed
Publication date: 2026/09/07
Wen YingZhang PengfeiLiao XinyuLiu JiankangZhang YangLiu Xuyun - Retinitis pigmentosa (RP) is the most common inherited retinal dystrophy (prevalence ~1:4000) and a leading Mendelian cause of working-age blindness. Despite marked genetic heterogeneity, its progression converges on a common secondary cascade of outer-retinal hyperoxia, increased reactive oxygen species (ROS), and mitochondrial dysfunction that drives cone degeneration and central vision loss. Because this oxidative cascade is largely genotype-independent and pharmacologically tractable, oxidative stress is a cross-cutting therapeutic target. Within it, mitochondrial DNA (mtDNA) is a key element: once released from damaged photoreceptors-free or within exosomes-it may act as a damage-associated molecular pattern (DAMP), engaging TLR9, cGAS-STING, and the NLRP3 inflammasome and sustaining chronic neuroinflammation. Extracellular mtDNA is therefore a potential integrative marker, simultaneously reflecting oxidative stress, mitochondrial dysfunction, cell death, and innate-immune activation. A central knowledge gap, however, remains: the mechanistic steps linking mtDNA to inflammation and to photoreceptor death have not been demonstrated in RP itself, and extracellular mtDNA has never been quantified in the ocular fluids of RP patients. In this review we appraise oxidative biomarkers in RP, propose extracellular mtDNA as a candidate biomarker of disease activity, and examine antioxidant and redox-modulating therapies-from N-acetylcysteine and elamipretide trials to DAMP-sensor inhibition-across experimental and clinical models. Finally, we propose extracellular mtDNA as a candidate pharmacodynamic endpoint and outline a path toward its validation. - Source: PubMed
Publication date: 2026/09/02
Grimaldi RossellaFranco FrancescaVingolo Enzo Maria