AGTRL1 Pre-design Chimera RNAi
- Known as:
- AGTRL1 Pre-design Chimera RNAi
- Catalog number:
- H00000187-R02
- Product Quantity:
- 10 nmol
- Category:
- -
- Supplier:
- Abno
- Gene target:
- AGTRL1 Pre-design Chimera RNAi
Related genes to: AGTRL1 Pre-design Chimera RNAi
- 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
Related products to: AGTRL1 Pre-design Chimera RNAi
Related articles to: AGTRL1 Pre-design Chimera RNAi
- : Aging is a major risk factor that exacerbates acute kidney injury (AKI) and subsequent renal fibrosis. However, age-related factors contributing to post-AKI fibrotic remodeling remain underexplored. This study aimed to investigate the protective potential of apelin, an endogenous peptide, in mitigating post-AKI renal fibrosis in aged mice. : A mouse model of AKI was established in 8-week-old and 19-month-old male C57BL/6 mice by clamping the left renal artery for 40 min, followed by reperfusion and euthanasia 2 weeks post-ischemia. To evaluate the protective effect of apelin pretreatment, the 19m-APLN group received intraperitoneal apelin administration (25 μg/kg/day) for 2 weeks prior to AKI induction. The effects of apelin on renal fibrosis were evaluated using renal function tests (blood urea nitrogen, serum creatinine levels), histological analysis, and Western blotting. : The 19m-AKI group exhibited more severe renal damage and interstitial fibrosis, along with a marked reduction in apelin and APLNR expression compared to the 8wk-AKI group. Apelin-13 pretreatment attenuated renal injury and fibrotic remodeling in aged mice, with reduced collagen deposition accompanied by lower pro-TGF-β1 expression and SMAD3 phosphorylation. : These results highlight the protective role of apelin against age-related exacerbation of post-AKI renal fibrosis, suggesting that prophylactic Apelin-13 administration may attenuate post-I/R renal injury and fibrotic remodeling in aged kidneys. - Source: PubMed
Publication date: 2026/09/10
Oh Won-SeokLee Sang GonKim Hyun TaeMoon Ji-HyunChoi Ah-LaHan Seung YunKim Do KyungLee Nam SeobJeong Young GilHong Geum-Lan - The aim of this study was to determine the applicability of dual activation of glucagon-like peptide-1 (GLP-1) and apelin (APJ) receptors as a next-generation therapeutic option for obesity and diabetes. - Source: PubMed
Publication date: 2026/09/18
Sridhar AnanyaaPalmer Ethan SCraig Sarah LTanday NeilO'Harte Finbarr P MIrwin Nigel - APLNR is a therapeutically important G protein-coupled receptor (GPCR) implicated in cardiovascular and metabolic regulation; however, how agonist binding reorganizes receptor dynamics to promote signaling competence remains poorly understood. Here, we used the small-molecule agonist CMF-019 as a representative ligand and integrated Gaussian accelerated molecular dynamics (GaMD), Markov state models (MSMs), and neural relational inference (NRI) to characterize the conformational dynamics, kinetic organization, and allosteric communication of APLNR in apo and CMF-019-bound states. We found that CMF-019 binding altered structural flexibility in extracellular and intracellular regions while modifying collective motions within the transmembrane core, indicating a transition toward a more signaling-permissive dynamic state. MSM analyses further revealed that CMF-019 binding redistributed APLNR toward activation-related intermediate conformations and accelerated transitions among metastable states. Mechanistically, NRI uncovered extensive rewiring of the receptor communication network, in which CMF-019 binding strengthened transmembrane coupling and redirected signal propagation toward more convergent signaling routes linked to intracellular functional regions. Together, these findings suggest that CMF-019 promotes APLNR signaling competence through integrated kinetic and allosteric remodeling, revealing a dynamic mechanism by which an agonist can reorganize receptor communication prior to downstream coupling. - Source: PubMed
Publication date: 2026/08/27
Dai HongZhu Jun-YaoZhang Bao-DanLiu Meng-TingSang PengYang Li-Quan - Neurofibromatosis type 2 (NF2)-associated meningiomas and schwannomas are vascular tumors, and while vascular endothelial growth factor (VEGF) inhibition with bevacizumab has benefited some NF2-related schwannomas, most NF2-associated meningiomas remain nonresponsive. - Source: PubMed
Publication date: 2026/08/17
Bhattacharyya SrirupaBeauchamp Roberta LRamesh Vijaya - The apelin/APJ system, a vital signal axis, regulates key physiological processes in multiple systems, including vascular permeability, inflammatory response and angiogenesis. However, in the pathophysiology of ocular neurovascular disorders, this signaling pathway exhibits dual functions that are highly dependent on the disease stage and microenvironment. Growing evidence suggests that during early disease stages, upregulation of the phosphoinositide 3-kinase/protein kinase B (PI3K/Akt) signaling pathway and downregulation of the NF-κB signaling cascade enable the system to exert vascular protection and neuroprotective effects. Conversely, in the late stages, stimulation by chronic hypoxia and ischemia strongly promotes pathological angiogenesis through the activation of the PI3K-Akt-mTORC1 and Ras-Raf-MEK-ERK cascades. Therefore, resolving this paradoxical behavior is essential for its clinical translation. Therefore, this review critically evaluates the stage-dependent dual roles of the apelin/APJ system in ocular neurovascular disorders. By utilizing ophthalmic diseases as highly representative and accessible models for the central nervous system, we dissect the molecular shift from vascular stability to pathological angiogenesis. Ultimately, as a disease stage biomarker and a novel therapeutic target for combating both systemic angiogenesis and neurodegeneration, we emphasize the translational potential of the apelin/APJ system. - Source: PubMed
Publication date: 2026/08/20
Sang SihanZhao HongboYu ZhiliuZhang YiquanJiang YanrongFeng Jing