Goat Anti-Human CD284, N-terminus
- Known as:
- Goat Antibody toHuman CD284, N-terminus
- Catalog number:
- 129-10142
- Product Quantity:
- 100
- Category:
- -
- Supplier:
- Ray Biotech
- Gene target:
- Goat Anti-Human CD284 N-terminus
Related genes to: Goat Anti-Human CD284, N-terminus
- 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: Goat Anti-Human CD284, N-terminus
Related articles to: Goat Anti-Human CD284, N-terminus
- (), a traditional medicinal plant widely used in Southeast Asia, has gained attention as a potential nutraceutical and therapeutic agent due to its diverse phytochemical composition, including phenolics, flavonoids, terpenoids, phytosterols, and sulfur-containing compounds. Growing evidence indicates that modulates key molecular pathways related to oxidative stress, inflammation, immune regulation, and cellular metabolism, such as NF-κB, TLR4, Nrf2, and p38 MAPK. This review summarizes recent advances in its phytochemistry, extraction methods, and pharmacological activities. The therapeutic potential of is discussed in cancer, metabolic disorders, infections, and bone diseases. However, further studies on bioavailability, safety, and clinical validation are required. - Source: PubMed
Publication date: 2026/06/01
Cheng Yi-LeCao LiangMajid MuhammadZeng Jun-HuangUllah HidayatZhang Xin-YiYuan XiaHu Xian-JingYang Mao-Xun - Autism spectrum disorder (ASD) is a neurological condition with growing global prevalence. One of the important factors involved in the pathophysiology of ASD is experiencing stress during early life, such as maternal separation (MS). Metformin, a well-founded glucose-lowering agent, possesses neuroprotective properties. This research aims to investigate the effects of metformin on autism-related behaviors in MS mice, with a focus on its probable effects on ameliorating hippocampal oxidative stress imbalance and neuroinflammation. In this study, 40 male mice were randomly assigned to five experimental groups. The control group received an intraperitoneal injection of normal saline (10 ml/kg), while normal saline (10 ml/kg) or metformin at doses of 100, 200, and 300 mg/kg were injected into the MS mice for 2 weeks. Behavioral trials, including the three-chamber sociability test, the shuttle box test, and the marble burying test (MBT) were conducted to evaluate autism-related behaviors. Malondialdehyde (MDA), nitrite, total antioxidant capacity (TAC), and expression of inflammatory cytokines including TLR4, TNF-α, IL-1β, and NLRP3 at the gene level were evaluated in the hippocampus. The results revealed that metformin enhanced the social preference index (SPI) and sociability index (SI) in the three-chamber test, improved passive avoidance memory in the shuttle box test, and reduced repetitive behaviors as assessed by the MBT. Furthermore, metformin decreased hippocampal levels of nitrite, MDA and the gene expression of inflammatory cytokines. In conclusion, metformin appears to alleviate autism-related behaviors in MS mice, possibly through combating oxidative stress imbalance and mRNA expression of inflammatory cytokines within the hippocampus. - Source: PubMed
Dehkordi Zahra VahedGhadiri MaryamAmini-Khoei Hossein - Spontaneous preterm birth (sPTB; delivery before 37 weeks) remains a leading cause of neonatal mortality, and intrauterine infection is implicated in a substantial proportion of cases. Emerging evidence links oral pathogens such as Porphyromonas gingivalis and Fusobacterium nucleatum to adverse gestational outcomes; however, the mechanistic pathways connecting chronic apical periodontitis (CAP) with gestational risk remain incompletely defined. In pregnant C57BL/6J mice, CAP was established by root canal inoculation and complemented by a tail-vein challenge model using bacterial suspensions (1 × 10 CFU/mL). Gestational length, placental histopathology, inflammatory markers, and bacterial DNA signals were assessed by qPCR. In parallel, human trophoblasts were exposed to P. gingivalis or F. nucleatum (MOI = 50, 24 h) to examine inflammatory signaling consistent with activation of the TLR4/MyD88/NF-κB axis. Relative to controls, CAP-associated groups showed gestational shortening (median 19.5 vs 20.5 days), accompanied by increased placental inflammatory readouts (including elevated IL-1β and TNF-α) and histopathological features consistent with inflammatory injury. qPCR further indicated the presence of bacterial DNA signals in placental and vascular tissues. In trophoblast assays, F. nucleatum elicited stronger proinflammatory responses than P. gingivalis, in association with increased NF-κB phosphorylation. Collectively, these findings suggest that CAP-associated oral pathogens may contribute to gestational shortening by driving placental inflammation via TLR4/MyD88/NF-κB signaling, supporting an oral-placental microbial axis as a potential target for mitigating infection-related gestational risk. - Source: PubMed
Publication date: 2026/05/15
Zhang YangyangWang XiaoheLi MengWu ZeyuLin JingYu XianmeiLi LingZhao Jin - Neuroinflammation is an important factor affecting the prognosis of ischemic brain injury and has become a potential target for stroke treatment. Resveratrol is a natural product with multiple biological activities, including anti-neuroinflammatory, anti-oxidative stress, and anti-apoptotic effects. This study focuses on the mechanism by which resveratrol protects neurological function after stroke by inhibiting neuroinflammation. A rat model of ischemic stroke was established through middle cerebral artery occlusion (MCAO). Neurological function was assessed via 2,3,5-triphenyltetrazolium chloride (TTC) staining, neurological deficit scoring, and immunohistochemical analysis. Animal behaviors were evaluated using the elevated plus maze, open field test, social interaction test, and sucrose preference test. Neuroinflammation was examined by measuring the expression of inflammatory factors including IL-6, IL-1β, and TNF-α. Oxidative stress was assessed by detecting the levels of glutathione (GSH), glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), and total antioxidant capacity (T-AOC). The expression of key proteins involved in neuroinflammation- and oxidative stress-related signaling pathways was examined by Western blotting. The results demonstrated that resveratrol effectively reduced neurological deficit scores, decreased cerebral infarct volume, and alleviated post-stroke cognitive impairment (PSCI) in rats. Additionally, resveratrol significantly suppressed neuroinflammation and improved antioxidant capacity. Further mechanistic investigations revealed that resveratrol markedly inhibited the TLR4/NF-κB/AIM2 signaling pathway while activating the NRF2/NQO1 pathway. In conclusion, this study demonstrates that resveratrol exerts anti-inflammatory and antioxidant effects, and protects neurological function by targeting the TLR4/NF-κB/AIM2 and NRF2/NQO1 signaling pathways. These findings provide a novel strategy for the neuroprotective treatment of stroke. - Source: PubMed
Publication date: 2026/05/15
Liufu ChunLin JinxuanZhang Hui - Keratinocyte migration is fundamental to re-epithelialization and the restoration of epithelial barrier integrity in the skin and oral mucosa, though it is highly susceptible to impairment by the bacterial inflammatory mediator lipopolysaccharide (LPS). We demonstrate that LPS-activated toll-like receptor 4 (TLR4) interacts directly with the focal adhesion scaffold paxillin to induce site-specific phosphorylation at Ser273. This signaling event promotes persistent Rac1 activation, which disrupts the adhesion turnover essential for coordinated migration. Functional validation using Ser273 paxillin mutants demonstrated that this site-specific phosphorylation is necessary and sufficient to drive migratory dysfunction. Furthermore, pharmacologic Rac1 inhibition suppresses paxillin phosphorylation and restores epithelial organization, revealing a bidirectional relationship between paxillin and Rac1 signaling. These findings define a TLR4-paxillin-Rac1 signaling axis that links inflammatory activation to focal adhesion remodeling, identifying Rac1-dependent adhesion dysregulation as a mechanistic driver of impaired epithelial repair. - Source: PubMed
Publication date: 2026/05/21
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