Goat Anti-GPR81 _ FKSG80, with HRP-conjugated secondary antibody
- Known as:
- Goat Antibody toGPR81 _ FKSG80, horseradish peroxidase-labelled secondary detector ab (anti-)
- Catalog number:
- 126-10102
- Product Quantity:
- 100
- Category:
- -
- Supplier:
- Ray Biotech
- Gene target:
- Goat Anti-GPR81 _ FKSG80 with HRP-conjugated secondary antibody
Related genes to: Goat Anti-GPR81 _ FKSG80, with HRP-conjugated secondary antibody
- Gene:
- HCAR1 NIH gene
- Name:
- hydroxycarboxylic acid receptor 1
- Previous symbol:
- GPR104, GPR81
- Synonyms:
- HCA1, FKSG80, TA-GPCR, LACR1
- Chromosome:
- 12q24.31
- Locus Type:
- gene with protein product
- Date approved:
- 2000-01-20
- Date modifiied:
- 2015-09-11
Related products to: Goat Anti-GPR81 _ FKSG80, with HRP-conjugated secondary antibody
Related articles to: Goat Anti-GPR81 _ FKSG80, with HRP-conjugated secondary antibody
- - Source: PubMed
Publication date: 2025/03/10
He JiachengChai XiaoleiZhang QiansenWang YangWang YijieYang XinyuWu JingboFeng BoSun JingRui WeiweiZe ShuyinFu YuanyuanZhao YumiaoZhang YingZhang YaoLiu MeizhenLiu ChuangShe MeifuHu XiangfeiMa XueyunYang HuaiyuLi DaweiZhao SenlinLi GuichaoZhang ZhenTian ZhonghuiMa YanlinCao LingyanYi BoLi DaliNussinov RuthEng CharisChan Timothy ARuppin EytanGutkind J SilvioCheng FeixiongLiu MingyaoLu Weiqiang - The diffusible gas nitric oxide (NO) and amino acid γ-gamma-aminobutyric acid (GABA) exert contrary effects on glucose counterregulation in the male rat, but how these neurochemical signals integrate within ventromedial hypothalamic nucleus (VMN) neural circuitries remains unclear. Female rat dorsomedial (VMNdm) and ventrolateral (VMNvl) GABAergic neurons express neuronal nitric oxide synthase (nNOS) mRNA; notably these subpopulations exhibit dissimilar nNOS transcriptional responses to insulin-induced hypoglycemia (IIH). Here, nNOS gene knockdown tools were used to examine whether one or both VMN GABA neuron groups may be a target for nitrergic control of basal and hypoglycemic counterregulatory hormone secretion in the male. Data show that VMN nNOS gene knockdown respectively up- or down-regulated counterregulatory hormone profiles in eu- versus hypoglycemic male rats. Single-cell multiplex qPCR analysis of laser-catapult-microdissected GABA neurons showed that IIH elevated nNOS gene expression in GABA neurons from each VMN division, yet nNOS siRNA pretreatment attenuated distinctive IIH-associated transmitter marker gene expression patterns in VMNdm versus VMNvl GABAergic neurons. nNOS gene silencing had similar effects on glucokinase and glucose transporter gene responses to IIH in each GABA neuron subpopulation but elicited division-specific effects on mRNA encoding 5-AMP-activated protein kinase (AMPK) alpha/catalytic subunits and the lactate membrane receptor GPR81/HCAR1. Current findings provide original evidence that VMN NO may impose bi-directional, glucose status-contingent control of counterregulatory hormone outflow in the male rat. Data moreover imply that during IIH, NO may control distinctive sources of metabolic sensory regulatory stimuli in VMNdm versus VMNvl GABA neurons and may shape unique counterregulation-controlling neurochemical transmission by each cell population. - Source: PubMed
Publication date: 2025/02/24
Roy Sagor CPasula Madhu BabuSapkota SubashBriski Karen P - Generation of reactive oxygen species is an important part of the innate immune response. Generating microbicidal levels of reactive oxygen species (ROS) requires adaptation of mucosal barriers. High tolerance of ROS provides improved innate immune defenses against pathogens, whereas low tolerance renders host cells prone to chronic toxicity and mutagenesis, which can promote inflammation (e.g., in asthma and Crohn's disease) and cancerogenesis. The mechanisms that sense and mediate host tolerance to ROS are little understood. In this study, we discover an unexpected role for the redox-sensitive, chemokine-like lipid 5-oxo-eicosatetraenoic acid (5-KETE) in redox adaptation. 5-KETE is known to attract leukocytes to damaged/infected mucosal barriers by signaling through its receptor, OXER1. Suggestive of a distinct non-immune function, we here report that the loss of the OXER1 ortholog Hcar1-4 causes barrier defects and baseline inflammation in the intestine of live zebrafish larvae. In zebrafish and cultured human cells, OXER1 signaling protects against oxidative nucleotide lesions by inducing DNA-protective Nudix hydrolases. Our data reveal the oxoeicosanoid pathway as a conserved ROS resilience mechanism that fortifies pathogen-exposed mucosal linings against increased oxidative stress . - Source: PubMed
Publication date: 2025/02/08
Lengyel MiklosMa YananGelashvili ZazaPeng SiyangQuraishi MeysoonNiethammer Philipp - The effacement of podocyte foot processes, which form slit diaphragms, are common features of proteinuria. Exploring podocyte energy metabolism, especially under diabetic conditions, may offer insights into the pathogenesis of diabetic kidney disease. Lipid accumulation is recognized as a cause of podocyte cytoskeleton remodeling and insulin resistance. Thus, the role of the metabolic sensor G-protein-coupled receptor 81 (GPR81) was examined in the molecular pathway of lipid accumulation in podocytes under hyperglycemic conditions. It was discovered that hyperglycemia downregulated the cyclic adenosine monophosphate/protein kinase A signaling pathway, which downregulated the expression of adipose triglyceride lipase (ATGL). Perilipin 1 was also downregulated; simultaneously, lipid droplet accumulation was enhanced. Glycerol and free fatty acid concentrations were also reduced, providing evidence of lipolysis inhibition. Interestingly, the expression of GPR81 decreased under hyperglycemia conditions despite the evidence of its activation, indicating strict lipolysis regulation. More importantly, cell functions were altered, reflected by an increase in albumin permeability and rearrangement of the actin cytoskeleton. The effect of ATGL activity inhibition on lipolysis, actin cytoskeleton arrangement, and permeability of the podocyte monolayer was investigated. The results were similar to GPR81 downregulation. Altogether, the present data indicate that GPR81 is likely a crucial part of the lipid sensing system, and its alterations during hyperglycemia might contribute to glomerular filtration barrier deterioration in diabetic kidney disease. - Source: PubMed
Grochowalska KlaudiaSzrejder MariaRachubik PatrycjaAudzeyenka IrenaRogacka DorotaNarajczyk MagdalenaPiwkowska Agnieszka - In this study, we examined the effect of GPR180, a G protein-coupled receptor (GPCR) family member, on lipid metabolism of adipose tissue. We used adeno-associated virus overexpression of in subcutaneous adipose tissue, adipocyte-specific knockout mice and stromal vascular fraction (SVF) cells to explore the role and mechanism of GPR180 in lipid metabolism in adipocytes. Levels of mRNA in subcutaneous and epididymal adipose tissues were significantly reduced in mice fed high-fat diet (HFD). Overexpression of in subcutaneous white adipose tissue (sWAT) improved lipid metabolism and protected mice from HFD-induced obesity. Conversely, adipocyte-specific knockout of exacerbated lipid metabolism disorders induced by HFD. In cultured adipocytes differentiated from SVF cells, GPR180 inhibited lipogenesis and fatty acid (FA) uptake. Collectively, our study reveals that GPR180 functions to suppress lipid accumulation in adipocytes. This study identifies GPR180 as a novel regulator of lipid metabolism and energy homeostasis. It demonstrates that GPR180 influences adipose tissue function, mitigates high-fat diet-induced obesity, and inhibits lipogenesis. Unique expression patterns and GWAS data linking GPR180 to lipid regulation highlight its systemic role. These findings establish GPR180 as a promising therapeutic target for metabolic disorders, warranting further research to uncover its molecular mechanisms and clinical applications. - Source: PubMed
Publication date: 2025/02/10
Zhu ZimingYang YaxuSun LijunZhang YunhuaHan XueLuo ChaoYin YueZhang Weizhen