Polyclonal Toll Interactin Protein (TOLLIP/TOLIP) (CT)
- Known as:
- Polyclonal Toll Interactin Protein (TOLLIP/TOLIP) (CT)
- Catalog number:
- pc-598
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Kamiya biomedical company
- Gene target:
- Polyclonal Toll Interactin Protein (TOLLIP/TOLIP) ()
Ask about this productRelated genes to: Polyclonal Toll Interactin Protein (TOLLIP/TOLIP) (CT)
- Gene:
- TLR4 NIH gene
- Name:
- toll like receptor 4
- Previous symbol:
- -
- Synonyms:
- hToll, CD284, TLR-4, ARMD10
- Chromosome:
- 9q33.1
- Locus Type:
- gene with protein product
- Date approved:
- 1998-06-25
- Date modifiied:
- 2016-01-21
Related products to: Polyclonal Toll Interactin Protein (TOLLIP/TOLIP) (CT)
Related articles to: Polyclonal Toll Interactin Protein (TOLLIP/TOLIP) (CT)
- Friedelin (FD), a natural pentacyclic triterpene, exerts neuroprotective effects, but its role in cerebral ischemic stroke remains unknown. In this study, FD attenuated middle cerebral artery occlusion and reperfusion (MCAO/R)-induced neurological deficits, reduced infarct volume, and inhibited neuronal apoptosis in mice. Additionally, FD suppressed proinflammatory microglial phenotype and proinflammatory cytokine secretion in oxygen-glucose deprivation and reoxygenation (OGD/R)-exposed BV2 cells and in mice after MCAO/R. FD alleviated HT22 cell injury after exposure to conditioned medium from BV2 cells subjected to OGD/R. A mechanistic exploration using network pharmacology and the finding that FD concentration-dependently suppressed nitric oxide (NO) overproduction induced by the Toll-like receptor 4 (TLR4)-specific ligand ultrapure LPS, identified TLR4 as a potential target of FD. FD suppressed proinflammatory microglial phenotype, proinflammatory cytokine secretion and ferroptosis by reducing TLR4 protein expression in mice after MCAO/R and in OGD/R-exposed BV2 cells. Inhibiting ferroptosis in BV2 cells ameliorated OGD/R-induced proinflammatory microglial phenotype and proinflammatory cytokine secretion. Thus, FD alleviated cerebral ischemic injury by repressing proinflammatory microglial phenotype through the regulation of TLR4-induced ferroptosis. - Source: PubMed
Publication date: 2026/07/23
Zhang HailinYuan GuoqiangDong ZhiqiangYang PengyuYang WenzhenLi Jianxiong - Ulcerative colitis (UC) remains a major therapeutic challenge. Although natural polysaccharides exhibit therapeutic potential, their structure-activity relationships are still unclear, which limits their clinical application. - Source: PubMed
Publication date: 2026/08/19
Li HuajianKe QiaoyingFeng JiaweiLiang TengZhang WanghaoYang BohanZhang ZiyiJiang LaiPiao Ji-GangWei Yinghui - Rheumatoid arthritis (RA) is a chronic autoimmune disorder characterized by synovial inflammation and joint destruction. Bone marrow mesenchymal stem cells (BMSCs) have shown therapeutic potential in RA, but the underlying mechanisms remain poorly understood. - Source: PubMed
Lian ShilinMa XiaoMeng YichenZhou Xuhui - Chronic diabetic wounds represent a significant clinical challenge due to impaired healing processes characterized by persistent inflammation, compromised angiogenesis, and a hostile microenvironment. Despite the therapeutic potential of mesenchymal stem cells (MSCs), their post-transplantation survival remains suboptimal in such pathological conditions. Here, we developed a sustained-release oxymatrine-loaded hyaluronic acid methacryloyl (HAMA) hydrogel to enhance placental mesenchymal stem cell (PMSC)-mediated repair in diabetic wounds. In a streptozotocin-induced diabetic mouse model with full-thickness dorsal skin defects, photo-crosslinked HAMA-OMT hydrogels were fabricated and evaluated for their effects on PMSC survival and wound healing outcomes. Comprehensive assessments included wound closure rates, histological analysis, angiogenesis, collagen remodeling, macrophage polarization, and the activation status of Nrf2/HO-1 and TLR4/NF-κB signaling pathways. The porous HAMA matrix provided structural support for PMSC adhesion and survival, while OMT incorporation improved hypoxia resistance and mitigated burst release kinetics. In diabetic wounds, the HAMA-OMT+PMSCs combination treatment significantly accelerated re-epithelialization, enhanced regeneration of hair follicles and sweat glands, promoted angiogenesis, and improved collagen organization compared to single-treatment groups. Mechanistically, OMT exerted dual regulatory effects by suppressing TLR4/NF-κB-driven inflammatory responses, promoting CD206M2 macrophage polarization, and activating Nrf2/HO-1-mediated antioxidant defenses, thereby protecting PMSCs from oxidative stress-induced apoptosis. Collectively, these findings demonstrate that OMT-loaded HAMA hydrogel synergizes with PMSCs to reconstruct a pro-regenerative microenvironment, offering a promising cell, material, and small-molecule combinatorial strategy for the effective treatment of chronic diabetic wounds. - Source: PubMed
Publication date: 2026/07/15
Liu LuLiu XiaodanLiu TingMa HaibinChen DongmeiLiu Shudan - Immunomodulators that simultaneously engage multiple pattern recognition receptors (PRRs) represent a promising strategy for shaping immune responses. Here we report the design and synthesis of covalently linked dual PRR agonists composed of a NOD1-selective ligand conjugated to agonists of TLR4, TLR7, or RIG-I. The resulting chimeric molecules were evaluated for receptor-specific agonist activation, immunomodulatory activity in human peripheral blood mononuclear cells, and adjuvant properties. In most cases, conjugation attenuated receptor agonist activity and reduced cytokine responses compared with mixtures of the corresponding unconjugated agonists. Despite modest activity, the conjugates, particularly the dual NOD1/TLR7 agonist, displayed robust adjuvant effects in a murine vaccination model. These results highlight the distinct immune signatures of conjugated NOD1-based dual agonists and support their development as next-generation vaccine adjuvants. - Source: PubMed
Publication date: 2026/06/15
Paradiso EmilianoJanež ŠpelaWeiss VeronikaFrkanec RužaJakopin Žiga