Polyclonal Rabbit EDG7 Antibody
- Known as:
- Polyclonal Rabbit EDG7 Antibody
- Catalog number:
- KA1136
- Product Quantity:
- 100ul
- Category:
- -
- Supplier:
- KareBay
- Gene target:
- Polyclonal Rabbit EDG7 Antibody
Related genes to: Polyclonal Rabbit EDG7 Antibody
- Gene:
- LPAR3 NIH gene
- Name:
- lysophosphatidic acid receptor 3
- Previous symbol:
- EDG7
- Synonyms:
- LP-A3, Edg-7, RP4-678I3, HOFNH30, LPA3
- Chromosome:
- 1p22.3
- Locus Type:
- gene with protein product
- Date approved:
- 2001-01-02
- Date modifiied:
- 2014-11-19
Related products to: Polyclonal Rabbit EDG7 Antibody
Related articles to: Polyclonal Rabbit EDG7 Antibody
- Phospholipase A (PLA) is a crucial enzyme in lipid metabolism and inflammatory signaling, playing a significant role in macrophage activation and neuroinflammation. However, its role in Japanese encephalitis virus (JEV)-mediated immune responses remains unclear. In this study, we show that PLA and its associated receptors, lysophosphatidic acid receptors (LPAR1 and LPAR3), are significantly upregulated at 24 h post-JEV infection, suggesting their involvement in JEV-induced inflammatory responses. To investigate the effect of PLA inhibition, we used arachidonyl trifluoromethyl ketone (AACOCF). Molecular docking using AutoDock Vina 1.1.2, supported by Protein Data Bank and AlphaFold structures, indicated that AACOCF interacts with key inflammatory targets including gp91 (- 7.9 kcal/mol) and LPAR3 (- 7.8 kcal/mol), suggesting its potential to modulate inflammatory and oxidative pathways. In vitro studies in JEV-infected macrophages demonstrated that AACOCF reduced activation of calcium-dependent cytosolic (c) PLA expression and phosphorylation, LPAR1, 3, MAPK signaling (JNK, ERK1/2, p38), and NF-κB protein levels, along with a reduction in JE viral RNA levels, likely reflecting indirect effects mediated through host pathway modulation. AACOCF also decreased proinflammatory cytokines (IL-1β, TNF-α) and autophagy-related markers (pAkt, LC3-II/I, SQSTM1/p6), and reduced expression of the ROS-generating enzyme gp91 (NOX2), indicating partial attenuation of inflammatory and oxidative stress-associated pathways. Oxidative stress was assessed via gp91 expression, and NF-κB was evaluated at protein level. These findings suggest that PLA contributes to JEV-induced inflammatory signaling, and that its inhibition modulates host responses during infection in vitro, rather than exerting a definitive therapeutic effect. - Source: PubMed
Publication date: 2026/05/26
Kumar AlokSingh GajendraZonta FrancescoZhu QiujieSingh AnjaliSaxena AbhishekGhosh Devlina - Intrauterine adhesions (IUA) are fibrotic scars that impair endometrial regeneration, and compromise fertility. Emerging evidence implicates circular RNAs (circRNAs) in fibrotic remodeling, but it remains unclear how the circRNA landscape and circRNA-associated splicing programs coordinately link uterine contractility, endometrial cell-cycle control, and immune activation in IUA. - Source: PubMed
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Chen YingqingJin JingXiang YingWang YanpingWu ShuangZhan NiXiong MengxinDeng Ali - Individuals with hypertension carry a high risk of stroke, which endangers human health. The study systematically elucidated the dynamic expression, functional effects, and molecular mechanisms of the circular RNA LPAR3 in ischemic stroke (IS). 300 essential-hypertension (EH) patients were enrolled, comprising 165 cases diagnosed with IS. mRNA abundance was quantified via RT-qPCR. C57BL/6 mice treated with MACO and Neuro-2a cells receiving oxygen-glucose deprivation/reoxygenation (OGD/R) were applied for functional experiments. Neurological deficits and infarct volume of mice were evaluated. Besides, key cellular behaviors encompassing proliferative capacity, apoptotic rate, and inflammatory response were monitored. The putative binding event was interrogated through luciferase reporter and RIP coupled to qPCR assays. A diminished level of circLPAR3 was evidenced in the plasma of IS patients, which can distinguish IS cases from EH and remains an independent predictor of patients' poor prognosis. In vivo, overexpression of circLPAR3 alleviated MACO-mediated neurological deficit and cerebral infarction. In vitro, OGD/R triggered the surge in cell apoptosis and pro-inflammatory cytokine release, but it was attenuated by circLPAR3 upregulation. Mechanistically, the neuro-rescue driven by circLPAR3 was offset by miR-634, whose plasma expression was negatively correlated with circLPAR3. KLB expression was significantly downregulated in cellular models and co-regulated by circLPAR3 and miR-634. circLPAR3/miR-634 modulates the pathological progression of IS by directly regulating neuronal apoptosis and orchestrating inflammatory responses, and KLB may serve as a key downstream target mediating the biological functions. - Source: PubMed
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Chen JinliYang JingWu QuanChen LilongWang HuiWu Junfeng - High-grade serous carcinoma (HGSC) is a remarkably heterogeneous tumor. The purpose of this study was to directly compare the reproducibility of transcriptomic profiles and biologically relevant molecular features across two spatial transcriptomics platforms-GeoMx Digital Spatial Profiler (GeoMx) and Visium Spatial Gene Expression (Visium) using AI-defined tumor regions associated with clinical outcome. - Source: PubMed
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