TLR2
- Known as:
- TLR2
- Catalog number:
- 000136A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- TLR2
Related genes to: TLR2
- Gene:
- TLR2 NIH gene
- Name:
- toll like receptor 2
- Previous symbol:
- -
- Synonyms:
- TIL4, CD282
- Chromosome:
- 4q31.3
- Locus Type:
- gene with protein product
- Date approved:
- 1998-06-25
- Date modifiied:
- 2016-10-25
Related products to: TLR2
Related articles to: TLR2
- Vascular smooth muscle cell (VSMC) dysfunction plays an important role in the pathogenesis of atherosclerosis. Chlamydia pneumoniae (C. pneumoniae) has been shown to infect and grow in VSMCs, and causes VSMC dysfunction, thereby promoting atherosclerosis development. However, it is an enigma how C. pneumoniae invades into VSMCs. In this study, we explored the specific mechanism of C. pneumoniae invading into VSMCs, and found that TLR2 expression and CXCR4 phosphorylation level were elevated after C. pneumoniae infection, and the translocation of TLR2 and CXCR4 to the membrane were increased at 15 min postinfection and reached the peak at 60 min, and then decreased at 180 min. The interaction between TLR2 and CXCR4 was enhanced in this process by co-immunoprecipitation and proximity ligation assays (PLA). The results from immunofluorescence staining demonstrated that C. pneumoniae invasion rate was dramatically decreased after knockdown of both TLR2 and CXCR4 compared with silencing of either TLR2 or CXCR4. Moreover, during C. pneumoniae invasion into VSMCs, the interaction between CXCR4 and β-arrestin2 was enhanced, and mutation of CXCR4 Ser339 resulted in the lack of β-arrestin2 recruitment. After TLR2 knockdown by siRNA, CXCR4 phosphorylation was decreased, and the translocation of CXCR4 to the membrane was abrogated, and CXCR4 was unable to recruit β-arrestin2 during C. pneumoniae invasion into VSMCs. In conclusion, C. pneumoniae invades into VSMCs through the CXCR4-β-arrestin2 pathway via TLR2/CXCR4 crosstalk, providing the first evidence for TLR2/CXCR4 interaction as well as receptor-mediated intracellular signaling that is exploited for C. pneumoniae invasion. - Source: PubMed
Publication date: 2025/09/27
Zhang YukeZhang LijunLi YiPan ShuangWang GuangyanZhang QiZhang Lijun - Mineralocorticoid receptor (MR) overactivation plays a crucial role in the pathogenesis of chronic kidney disease, as well as several cardiovascular and arterial diseases. Current studies determined the mechanisms of the beneficial kidney effects of the non-steroidal MR antagonist Finerenone (FN) in a mouse model of western diet-induced obesity and insulin resistance. 10-week-old male C57BL/6J mice were fed a low fat (LF) or a western diet (WD) for 12 weeks followed by treatment with either vehicle or finerenone (FN) for another 14 weeks (intervention studies) until they were 36 weeks old. Finerenone treatment prevented a) the increased albuminuria and kidney injury molecule 1 (KIM1), b) the expanded extracellular mesangial matrix and synaptopodin coverage, c) fibronectin, collagen IV , CD45 and CD68 immunostaining, d) glomerular basement membrane disruption, podocyte foot processes effacement, and mitochondrial structural abnormalities, e) the pro-inflammatory cytokines (MCP1), innate immunity pathways (TLR2, STING, STAT3), and fibrosis markers fibronectin, TGFβ and Pai1, and f) the increased kidney cholesterol levels. There was also reduced expression of nuclear receptor ERRγ without changes in ERRα in WD-fed mice whereas both ERRα and ERRγ expression levels increased after Finerenone treatment. NADH lifetime analysis showed decreased bound NADH, compatible with decreased mitochondrial OXPHOS in the kidneys of WD-fed mice compared to controls, which was prevented by finerenone treatment. In conclusion, Finerenone treatment exhibits a renal protective role and prevents the progression of kidney disease by regulating mitochondrial function, most likely via ERRγ, and reducing lipid accumulation and inflammation. - Source: PubMed
Publication date: 2025/09/29
Myakala KomuraiahWang Xiaoxin XShults NataliiaHughes Elenide Carvalho Ribeiro PatriciaPenjweini RozhinLink Katie ABarton KeelyKrawczyk EwaClarkson-Paredes CherylPopratiloff AnastasKnutson Jay RCowart L AshleyLevi Moshe - Periodontitis poses challenges in both early detection and late-stage treatment. The purpose of this study was to understand the role and mechanism of the lncRNA LBX2-AS1 in periodontitis. - Source: PubMed
Publication date: 2025/09/29
Liu FangQian ChengWang WenruiZhang RongxiuXu LiLiu Liang - Severe fever with thrombocytopenia syndrome (SFTS), an emerging infectious disease caused by a novel bunyavirus, presents a significant threat due to its high mortality rate. Immune suppression is recognized as a crucial factor in the progression of this disease. NK cells, as effector cells in the innate immune system, play important immune functions. Toll-like receptors (TLRs), specifically pattern-recognition receptors, initiate the activation of intracellular signaling factors upon activation. However, there is a paucity of data regarding immune responses in SFTS. In this study, we aimed to investigate the changes in TLR2 and NF-κB within NK cells and examine how the TLR2/NF-κB signaling pathway affects NK cells during SFTS. Our findings revealed that in SFTS patients, there was an increase in the expression of TLR2 and NF-κB in both CD56dimCD16+ and CD56brightCD16- NK cell subsets. Additionally, the function of CD56bright NK cells was enhanced in SFTS patients after stimulation with Pam3CSK4. This suggests that TLR2 signaling plays a crucial role in activating and enhancing the function of CD56bright NK cells following SFTS virus infection. This research will facilitate a deeper understanding of the pathogenesis of SFTSV and could provide an immunological foundation for developing new therapeutic strategies. - Source: PubMed
Publication date: 2025/09/27
Li Meng-MengYue Hao-RanWang JingXiong YanCao Ming-BoLiu Le-Le - Spinal cord injury (SCI) is a severe nervous trauma and the underlying mechanism of miR-1287-5p in its pathogenesis remains incompletely elucidated. - Source: PubMed
Publication date: 2025/09/26
Du RunzeLi YingnanWang Gang-GangLin Weicheng