APLNR ELISA kit
- Known as:
- APLNR Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- DL-APLNR-Ra
- Product Quantity:
- 96T
- Category:
- Elisa Kits
- Supplier:
- WDSTD
- Gene target:
- APLNR ELISA kit
Related genes to: APLNR ELISA kit
- Gene:
- APLNR NIH gene
- Name:
- apelin receptor
- Previous symbol:
- AGTRL1
- Synonyms:
- FLJ90771, APJ, APJR
- Chromosome:
- 11q12.1
- Locus Type:
- gene with protein product
- Date approved:
- 1994-07-07
- Date modifiied:
- 2014-11-19
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- Allergic airway inflammation (AA) is primarily driven by the activation of mast cells and eosinophils, with granular exocytosis serving as a key source of pro-allergic mediators that amplify pathological responses. This unmet need highlights the importance of identifying novel, pathway-specific therapeutic targets to improve disease management. A dust mite extract (DME)-induced murine model of AA was used to assess intranasal A13 (1 mg/kg daily) efficacy; human EoL-1 eosinophils and murine P815 mast cells were stimulated with PMA/ionomycin (P&I) to induce exocytosis. In DME-induced murine AA, intranasal A13 reduced lung inflammation by 58% (p < 0.01), serum sIgE by 73% (p < 0.001), and BALF Th2 cytokines (IL-4/IL-5/IL-13) by 65%-80% (p < 0.001), while restoring BALF IFN-γ (p < 0.01). A13 inhibited granular mediator release: in P&I-challenged WT mice, it reduced BALF eosinophil peroxidase (EPX) by 81% and mast cell protease-1 by 85%, but had no effect in APLNR⁻⁻ mice (p > 0.05). Mechanistically, P&I induced Rab27a upregulation (P815: 3.2-fold; EoL-1: 2.8-fold), which A13 reversed in vitro; in vivo, A13 lowered lung granulocyte Rab27a by 2.5-3.1-fold (p < 0.001). A13 engaged APLNR to recruit FBXO28, promoting K48-linked Rab27a ubiquitination and proteasomal degradation. APLNR knockdown or MG132 treatment abrogated A13's effects, while A13 enhanced FBXO28-Rab27a complex formation by 4.7-fold (p < 0.001)-an interaction undetectable in APLNR cells. Intranasal A13 exhibits localised action, effectively suppressing allergic inflammation without broad systemic immunosuppression, making it a promising candidate for development as a topical biologic to treat allergic airway diseases. - Source: PubMed
Publication date: 2026/05/01
Wu GaohuiYe YanyuDuan JiaqiLi MinyaoLiao YunYang PingchangHuang QinmiaoLiu Yu - Fetal growth restriction increases adverse pregnancy outcomes including preterm birth and intrauterine death. Apelin is a secreted peptide expressed in placental syncytiotrophoblast and downregulated in fetal growth restriction. We tested the hypothesis that adverse pregnancy outcome is associated with low maternal plasma apelin at diagnosis of early-onset fetal growth restriction. - Source: PubMed
Publication date: 2026/04/23
Braun NathalieBethell KatherineChaloner LydiaMaksym KatarzynaSpencer Rebecca NMaguire Janet JDavenport Anthony PDavid Anna LVaughan Owen R - Sustained macrophage-driven inflammation critically exacerbates post-infarction myocardial injury and remodeling. While Apelin-13 (A13) is known for its cardiovascular benefits, its direct immunomodulatory role on macrophages after myocardial infarction (MI) remains undefined. - Source: PubMed
Publication date: 2026/04/23
Xu Xian-JieShen KuoMa Yu-JieZhang Xiao-LiWang QiLiu PengHe Qi-FenWang Xian-QiXu Ya-NanFu He-LiangYang Ke-XunLi Jun-JieLuo Zheng-Xue - Current evidence show that exercise has beneficial effects on skeletal muscle function in individuals with chronic kidney disease (CKD). The STAT3 signaling pathway and the apelin axis (apelin receptor, APLNR- and ligands, -apelin and/or -elabela), participate in the processes of kidney inflammation and fibrosis and both may be involved in muscle wasting during CKD. Herein we report that STAT3 pathway and APLNR are in fact involved in the muscle impairment concomitant to CKD in experimental model and in adult individuals with CKD. Male BALB/c mice were first submitted to an 8-week ladder climbing resistance training (RT) protocol and further were submitted to doxorubicin-induced experimental CKD with or without use of the STAT3 inhibitor (Stattic). The GSE157712 dataset was used to assess the muscle transcriptome profile of CKD patients. Bioinformatics' analysis of gene set enrichment analysis (GSEA) and gene ontology (GO) were performed and the APLNR was found to be a central component of muscle response over kidney stress. Mice from the RT protocol showed a protective effect of blocking STAT3 against kidney and muscle injury markers, while both CKD individuals and CKD mice reported alterations in the APLNR muscle expression. In conclusion, the muscle tissue function is affected during CKD, which can be attenuated by a protective and synergistic effect of exercise and STAT3 inhibition. Thus, APLNR appears as a key gene associated with muscle dysfunction in CKD patients and its muscle expression can be regulated by resistance exercise. - Source: PubMed
Publication date: 2026/04/13
Pereira Gabrielde Oliveira Santos Thabata CarolineArioni Sofía TomaselliSeibt Pietra ManciniDos Santos Emily PereiraFortuna LuanaLazzarotto RodrigoZazula Matheus FelipeAgudelo Juan Sebastian HenaoResende E Silva Débora Tavares dePerez Hurtado Elizabeth CristinaNaliwaiko KatyaFernandez RicardoAlmeida Danilo Cândido dePereira Rafael Luiz - Anthracycline-induced cardiotoxicity remains a major clinical challenge, often progressing to heart failure years after therapy. Conventional cardioprotective agents, including angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, and beta-blockers, are widely used to preserve cardiac function; however, their effectiveness is limited by their inability to comprehensively address the complex, multifactorial pathophysiology of anthracycline-induced cardiotoxicity. This underscores the critical need for more effective and mechanism-based cardioprotective strategies that directly target the underlying molecular mechanisms, particularly oxidative stress and mitochondrial dysfunction. In recent years, the apelin-APJ signalling axis has attracted increasing attention as a potential therapeutic target in cardiovascular diseases owing to its multifaceted biological actions, including positive inotropy, vasodilation, anti-inflammatory, anti-fibrotic, anti-apoptotic, antioxidant, and pro-angiogenic effects. These pleiotropic actions are primarily mediated through the activation of key signalling pathways such as phosphoinositide 3-kinase/protein kinase B, extracellular signal-regulated kinases 1/2, and AMP-activated protein kinase. Given that these signalling cascades are disrupted during anthracycline-induced cardiotoxicity, pharmacological activation of the apelin-APJ axis may represent a promising avenue to mitigate anthracycline-associated cardiac injury with greater efficacy than conventional therapies. While native apelin isoforms (apelin-12, -13, -17, and [Pyr¹]apelin-13) are limited by their short half-lives, chemically modified analogues such as LIT01-196 and apelin-17(A2) exhibit enhanced stability and efficacy, with demonstrated cardioprotective effects in preclinical cardiovascular models and patients with chronic heart failure. However, their therapeutic potential in anthracycline-induced cardiotoxicity remains largely unexplored. This review highlights its promise as a novel cardioprotective strategy for mitigating anthracycline-induced cardiotoxicity. - Source: PubMed
Publication date: 2026/04/17
Desai Varsha G