Ask about this productRelated genes to: GRK4 antibody
- Gene:
- GRK4 NIH gene
- Name:
- G protein-coupled receptor kinase 4
- Previous symbol:
- GPRK2L
- Synonyms:
- GPRK4
- Chromosome:
- 4p16.3
- Locus Type:
- gene with protein product
- Date approved:
- 1993-10-14
- Date modifiied:
- 2015-09-07
Related products to: GRK4 antibody
Related articles to: GRK4 antibody
- - Source: PubMed
Publication date: 2026/04/21
Hua RuifangSu ZhaohaiLin XiangZeng GuozhongYang JiangyongWu TianzhuHe WenxiuJiang FuchengHuang WeihanWang MengyaoWang JichongLin DuFeng YunPei Fang - High-altitude hypoxia is a well-established risk factor for acute kidney injury (AKI), yet effective therapeutic options remain scarce. Salidroside, the primary active compound extracted from Rhodiola, has been reported to protect against hypoxia-induced damage in various organs. Here, we aimed to determine whether salidroside could alleviate kidney injury caused by acute high-altitude exposure and to investigate its underlying mechanisms. To this end, male Sprague-Dawley rats were exposed to hypobaric hypoxia simulating an altitude of 5000 meters and were treated with different doses of salidroside. Kidney injury biomarkers, including neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule-1 (KIM-1), and cystatin C (Cys-C), were measured in serum and urine. Histological analysis and protein expression levels of dopamine D1-like receptor (DRD1) and G protein-coupled receptor kinase 4 (GRK4) were also evaluated. In parallel, primary renal proximal tubular (RPT) cells from rats were cultured under hypoxic conditions to validate the findings in vitro, with additional groups receiving DRD1-targeting siRNA or the DRD1 agonist fenoldopam. Salidroside significantly reduced biomarker levels of kidney injury in vivo, preserved DRD1 expression, and inhibited GRK4 upregulation in a time- and dose-dependent manner. Likewise, in vitro treatment with salidroside enhanced cell viability and decreased apoptosis while restoring DRD1 levels and downregulating GRK4. Notably, the protective effects were abolished by DRD1 knockdown and enhanced by fenoldopam, indicating a DRD1-dependent mechanism. Molecular docking analysis further supported these results by demonstrating strong binding affinities between salidroside and both DRD1 and GRK4. Together, our findings suggest that salidroside attenuates hypoxia-induced renal injury through modulation of intrarenal dopamine signaling and highlight its potential as a preventive or therapeutic agent for individuals exposed to hypobaric hypoxia. - Source: PubMed
Publication date: 2026/03/31
Huan ChengZhilin GanDan XiaoYue WangXianglian LiLiwen MoYue Cheng - G protein-coupled receptor kinase 4 (GRK4) plays a vital role in the regulation of blood pressure. Several GRK4 gene variants have attracted attention because of their association with hypertension. However, the role of GRK4 R65L in hypertension is still unclear. In the present study, we report that global and renal tubule-targeted GRK4 R65L over-expression in mice caused salt-sensitive hypertension, accompanied by a rightward shift of the plot of urine sodium excretion against systolic blood pressure, that were improved by AAV9-mediated renal GRK4 depletion. RNA sequencing showed that the expression of the long chain L-2-hydroxyacid oxidase 2 (Hao2) gene ranked first in up-regulated candidates involved in the regulation of sodium-water metabolism. The salt-sensitive hypertension and increased renal oxidative stress in GRK4 R65L mice were mitigated by AAV9-mediated renal Hao2 depletion or administration of the potent antioxidant tempol. Immunoprecipitation-mass spectrometry showed an increased interaction between triosephosphate isomerase 1 (TPI1) and GRK4 in the kidneys of high salt-fed GRK4 R65L mice, accompanied by increased TPI1 phosphorylation and nuclear translocation, which were decreased, along with renal Hao2 expression, after GRK4 depletion. Renal H3K27ac levels and binding to the Hao2 promoter were increased but the levels of nuclear dihydroxyacetone phosphate (DHAP), a downstream molecule of TPI1, were decreased in high salt-fed GRK4 R65L mice. DHAP reduced the levels of H3K27ac and Hao2 in GRK4 R65L transfected-HK-2 cells. The H3K27ac inhibitor C646 mitigated the salt-sensitive hypertension in GRK4 R65L mice, accompanied by decreased H3K27ac and Hao2 expressions, and oxidative stress. Our results demonstrated that in high salt fed-GRK4 R65L mice, elevated renal TPI1 nuclear phosphorylation decreased DHAP levels and increased H3K27ac expression, which increased Hao2 expression and oxidative stress, caused a rightward shift of the pressure-natriuresis plot, and subsequently caused salt-sensitive hypertension. - Source: PubMed
Publication date: 2025/12/15
Zhang FuweiWan JindongJiang LianghongLin XiaoqianChen LinShao MuqingChen JiayaoWang LuningZheng ShuoRen HongmeiChen CaiyuJose Pedro AZeng ChunyuYang Jian - Ambient fine particulate matter (PM2.5) is a major environmental risk factor for hypertension, yet the renal sodium-handling mechanisms remain incompletely understood. This study investigates the role of G protein-coupled receptor kinase 4 (GRK4) and its downstream signalling axis in PM2.5-induced hypertensive pathogenesis. - Source: PubMed
Publication date: 2025/12/10
Lu XiYang TeJiang JiahuiJiang TaoLiu DanSu LiLi Yong - Hypertension, a major risk factor for cardiovascular diseases, is closely associated with excessive sodium intake and affects millions globally. Omentin-1, an adipokine with anti-inflammatory and antioxidant properties, has been implicated in blood pressure regulation, but its role in salt-sensitive hypertension remains unclear. This study investigated the antihypertensive and renal protective effects of omentin-1 in a deoxycorticosterone acetate (DOCA)-salt hypertensive rat model. We demonstrated that Omentin-1 overexpression significantly reduced blood pressure and attenuated renal dysfunction in DOCA-salt hypertensive rats, as evidenced by decreased serum creatinine (Scr) and blood urea nitrogen (BUN) levels, reduced renal fibrosis, and improved histopathological scores. Mechanistically, Omentin-1 downregulated angiotensin II type 1 receptor (ATR) expression in the kidney, which was associated with reduced G protein-coupled receptor kinase 4 (GRK4) levels. Further analysis revealed that omentin-1 suppressed GRK4 expression via the reactive oxygen species (ROS)/c-Myc signaling pathway. Overexpression of GRK4 abolished the antihypertensive and renal protective effects of omentin-1, confirming GRK4 as a key mediator in this process. These findings highlight omentin-1 as a potential therapeutic target for salt-sensitive hypertension, offering dual benefits in blood pressure reduction and renal protection through the ROS/c-Myc/GRK4/ATR axis. - Source: PubMed
Publication date: 2025/10/27
Hua RuifangSu ZhaohaiLin XiangZeng GuozhongYang JiangyongWu TianzhuHe WenxiuJiang FuchengHuang WeihanWang MengyaoWang JichongLin DuFeng YunPei Fang