Polyclonal Rabbit ALOX5 (Phospho-Ser523) Antibody
- Known as:
- Polyclonal Rabbit ALOX5 (Phospho-Ser523) Antibody
- Catalog number:
- KA0195
- Product Quantity:
- 100ul
- Category:
- -
- Supplier:
- KareBay
- Gene target:
- Polyclonal Rabbit ALOX5 (Phospho-Ser523) Antibody
Related genes to: Polyclonal Rabbit ALOX5 (Phospho-Ser523) Antibody
- Gene:
- ALOX5 NIH gene
- Name:
- arachidonate 5-lipoxygenase
- Previous symbol:
- -
- Synonyms:
- 5-LOX
- Chromosome:
- 10q11.21
- Locus Type:
- gene with protein product
- Date approved:
- 1992-07-10
- Date modifiied:
- 2016-10-05
Related products to: Polyclonal Rabbit ALOX5 (Phospho-Ser523) Antibody
Related articles to: Polyclonal Rabbit ALOX5 (Phospho-Ser523) Antibody
- The major challenge in the clinical treatment of gastrointestinal mucosal injury caused by high-altitude hypoxic environments lies in its unclear underlying mechanisms. In the previous study, we found that hypoxia-induced gastric and small intestinal damage was mainly attributable to ferroptosis mediated by hypoxia-inducible factor-α (HIF-α; mainly HIF-1α and HIF-2α). Both plant exosome-like nanoparticles and Lam. have been reported to have antioxidant properties. In the present study, orally delivered Lam. exosome-like nanoparticles (AELNs) reduced HIF-1α expression and alleviated gastric and small intestinal mucosal ferroptosis induced by hypoxia. We analyzed the compositions of AELNs and hypothesized that ipriflavone was the effector component, as it showed the highest abundance of metabolites. Subsequent experiments demonstrated that ipriflavone downregulated polyunsaturated fatty acid-phospholipids, NADPH oxidase 4 (NOX4), and arachidonate 5-lipoxygenase (ALOX5) by inhibiting HIF-α, consequently alleviating hypoxia-induced gastric and small intestinal mucosal ferroptosis. Ipriflavone was found to inhibit HIF-α by targeting prolyl hydroxylase domain protein 2 (PHD2) to induce it to hydroxylate HIF-α. This study highlights that ipriflavone, a potent HIF-α inhibitor, significantly ameliorates the gastric and small intestinal mucosal damage caused by hypoxia and has promise in clinical applications for treating disorders characterized by high levels of HIF-α. - Source: PubMed
Publication date: 2026/04/09
Wang DezhiLiao XingchenWang YilinWang XuexinZhang HengZeng JieZhang MingjieWang XinRen FangliWang YinyinLi MengWang WenchenLin QingGu LingyunChang ZhijieSheng Jianqiu - Ferroptosis, a regulated form of cell death, plays a critical role in renal tubular epithelial cells during acute kidney injury (AKI). Scoparone, a bioactive coumarin, confers organ protection in cardiovascular, hepatic, and inflammatory disorders. However, its therapeutic potential in AKI and its role in regulating ferroptosis remain unexplored. This study aimed to investigate the role of scoparone in cisplatin-induced AKI using mouse models and human renal tubular epithelial (HK-2) cells. Integrative analyses, incorporating network pharmacology, bioinformatics, and machine learning, identified arachidonate 5-lipoxygenase (ALOX5) as a key target. In vivo, scoparone treatment markedly improved renal function and preserved histopathological architecture in cisplatin-induced AKI mice. In vitro, scoparone attenuated cisplatin-induced cytotoxicity in HK-2 cells without compromising cisplatin's antitumor efficacy in four human tumor cell lines. Mechanistically, scoparone downregulated ALOX5, suppressed lipid peroxidation, and inhibited ferroptosis. Pharmacological inhibition of ALOX5 with zileuton recapitulated these protective effects, with no additional benefit from co-treatment. Altogether, the findings of this study show that scoparone ameliorates cisplatin-induced AKI by suppressing ALOX5-mediated ferroptosis, positioning ALOX5 as a potential therapeutic target and supporting scoparone as a promising therapeutic candidate for AKI management. - Source: PubMed
Publication date: 2026/04/10
Dai CongcongHuang ShutingHuang NaMu SuwanLiu SuwangXie MinhuiMei JingTang YuhongYu HonghaoYue PengpengLi YongOu Jun - This study aims to elucidate the role and underlying mechanisms of arachidonate 5-lipoxygenase (ALOX5) in osteoarthritis (OA) to identify novel therapeutic targets for this disease. - Source: PubMed
Publication date: 2026/04/10
Cheng GangChen KaiwenWang ZhigangChen HuihaiShen Yixin - Alzheimer's disease (AD) is a multifactorial neurodegenerative disorder characterized by coordinated dysfunction across multiple brain cell types. Natural compounds with multi-target regulatory potential represent promising therapeutic candidates, yet their cell-type-specific mechanisms in the human AD brain remain incompletely understood. In this study, we integrated ligand-based target prediction with large-scale single-nucleus RNA sequencing (snRNA-seq) data from 201,074 nuclei obtained from AD and control human brain samples, together with subcluster-level functional profiling, cell-cell communication analysis, transcriptional regulatory network inference, and structure-based molecular docking and molecular dynamics simulations to systematically characterize the multicellular actions of isofraxidin. Our analyses identified 19 high-confidence isofraxidin targets exhibiting distinct enrichment patterns across AD-associated cell populations. Key targets-including ALOX5 in microglia, MAOB in astrocytes, HSPA1A in endothelial cells (EC), and CBR1 in oligodendrocytes (ODC)-were preferentially localized to disease-relevant cellular subclusters. snRNA-seq revealed marked remodeling of these cell types in AD, characterized by inflammatory microglia, reactive astrocytes, stress-impaired ECs and neurodegeneration-associated ODCs, which overlapped with the highest target enrichment. Functional and regulatory analyses indicated that these vulnerable states converge on oxidative stress, metabolic dysregulation, proteostasis impairment, and aberrant inflammatory signaling. Molecular docking and 100-ns molecular dynamics simulations further confirmed stable and energetically favorable binding of isofraxidin to its core targets. Collectively, this integrative single-cell framework delineates the cell-type-specific therapeutic landscape of isofraxidin in AD and highlights its potential to coordinately modulate key pathogenic pathways underlying neurodegeneration. - Source: PubMed
Publication date: 2026/04/08
Gong XinXu ChengfeiChen XinguiWang Kai - Carotid atherosclerosis is a significant cause of ischemic stroke. It is a chronic inflammatory disease characterized by the progressive accumulation of inflammatory cells and mediators. Specific key metabolites are known to play pivotal roles in the progression of atherosclerosis. By applying spatial omics, we pinpointed the colocalization of arachidonic acid with inflammatory cells in plaques, providing direct spatial evidence for its pro-inflammatory role in atherosclerosis. - Source: PubMed
Publication date: 2026/03/25
Wan JiaxinLin RijinJiao ZhouyangCao HuiZhang ChuangZhang XiaowenFan MengyanZhang NanZhang JiameiLiu HuixiangZhang YikeHuang ChenYang JianglinLi JingZhang JieGuan Sheng