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
- This narrative review aimed to critically synthesize and evaluate the current evidence on the roles of TIR domain-containing adaptor protein in tumorigenesis and cancer progression, with a particular focus on elucidating the underlying inflammatory and immune regulatory mechanisms mediated by toll-like receptor signaling. A targeted literature search of recent studies (2015-2024) was performed using PubMed and Web of Science. Classic foundational publications (1998-2014) were supplemented through reference tracking. We included experimental, cellular, and clinical studies focusing on TIR domain-containing adaptor protein in cancer. The synthesized findings indicate that TIR domain-containing adaptor protein has been implicated in malignant progression in bladder, pancreatic, and gastric cancers by sustaining chronic inflammation and shaping an immunosuppressive tumor microenvironment through the TLR2/4-MyD88-NF-κB/MAPK axis, whereas it may exert homeostatic and protective effects in colorectal cancer. TIR domain-containing adaptor protein activity is tightly regulated by cellular origin, ligand specificity, and epigenetic modifications such as promoter methylation, which are closely associated with cancer risk and disease severity. TIR domain-containing adaptor protein serves as a critical regulator in inflammation-driven tumors with distinct context-dependent functions and represents a promising biomarker and therapeutic target. Further research focusing on its precise regulatory mechanisms and cell-specific targeted strategies will facilitate its clinical translation. - Source: PubMed
Publication date: 2026/08/17
Jiang HuihuiZhang RuiDing ShanshanYu ZhenQi ChenruiMeng JinWang Lu - Neurological disorders are a major global health challenge in the current era, and they need new therapeutic treatments. - Source: PubMed
Al Hasan Md SakibShahria NazninEmon YasinAlshahrani Mohammad YMia EmonAltemani Faisal HSuma Rituparna BiswasSumaya Umme HabibaUddin Mohammed BurhanIslam Md Torequl - Unlike adult hearts, neonatal hearts can regenerate and adapt to stress. To identify both cardioprotective and regenerative mechanisms, we compared activated genes and related signaling pathways in the neonatal mouse heart after myocardial infarction (MI) and after exposure to pressure overload using a neonatal model of transverse aortic constriction (nTAC) at postnatal day 1 (P1). We identified three immune-related genes-Ccl4, S100a8, and C1qa-of high interest, as they encode secreted factors, are highly expressed in the neonatal mouse heart in both injury types, and their receptors are expressed on neonatal cardiomyocytes (nCM) and cardiac endothelial cells (EC). We investigated their effects on primary mouse EC and nCM in vitro. Our study found that the combination of these secreted factors (Pool3) enhances EC and nCM cell cycle re-entry and reduces the rate of apoptosis. Combined in vivo and in vitro transcriptome analyses revealed that Toll-like receptor 2 (TLR2) activation in nCM induces a shared pro-survival and cell cycle re-entry-associated signaling, including upregulation of Bcl2 and Birc5, respectively. The direct and pivotal role of TLR2 in enhancing nCM cell cycle re-entry and survival was further confirmed using TLR2 knockout (KO) nCM, a TLR2 inhibitor, and a TLR2 agonist (zymosan). Moreover, the importance of TLR2 in mediating the adaptive response to pressure overload in neonatal mice was confirmed in TLR2 KO mice, which failed to adapt to pressure overload and exhibited high mortality together with maladaptive cardiac remodeling as early as 7 days post-surgery. Collectively, these findings demonstrate that TLR2 is essential for mediating nCM cell cycle re-entry, survival, and adaptive/regenerative response to injury. - Source: PubMed
Publication date: 2026/08/14
Nicke JuliaGoldspink AdrianMenn MalteFleischmann Bernd KMalek Mohammadi Mona - Toll-like receptor 2 (TLR2) is a cell-surface pattern-recognition receptor that contributes to inflammatory signaling and represents an accessible target for extracellular protein binders. Here, we integrated phage-display screening, biophysical characterization, comparative protein-protein docking, in silico perturbation, and cellular assays to characterize scFv33, a TLR2-binding single-chain variable fragment. scFv33 showed nanomolar binding to recombinant TLR2 and preferential recognition over the tested receptor comparator. Independent docking workflows converged on a CDR-centered recognition model in which heavy- and light-chain CDRs form a distributed network of charged, polar, and aromatic contacts across the TLR2 leucine-rich-repeat surface. Targeted computational perturbation further supported the sensitivity of this recognition model to changes on both the binder and receptor sides. In Pam3CSK4-stimulated microglial cells, scFv33 attenuated pro-inflammatory cytokine transcription. Together, these findings establish scFv33 as a functional TLR2-directed antibody fragment and provide an experimentally testable framework for structure-informed optimization of innate immune receptor binders. - Source: PubMed
Publication date: 2026/08/14
Park Jun SeoLee SubeenJeon JaekyungLee HyunjiLee Sung Joong - - Source: PubMed
Luo HaodangZeng QianruiXie NaZhang ChiLiu ChangChen ShutongYan CaihongLi ChunWu HaiyingHe JunZeng YanhuaYou Xiaoxing