GPR182 _ ADMR Rabbit antibody Ab Aff - Purified
- Known as:
- GPR182 _ ADMR Rabbit (anti-) Antibody Aff - Purified
- Catalog number:
- AP06929PU-N
- Product Quantity:
- 50
- Category:
- -
- Supplier:
- ACR
- Gene target:
- GPR182 _ ADMR Rabbit antibody Aff - Purified
Related genes to: GPR182 _ ADMR Rabbit antibody Ab Aff - Purified
- Gene:
- GPR182 NIH gene
- Name:
- G protein-coupled receptor 182
- Previous symbol:
- ADMR
- Synonyms:
- hrhAMR, G10D, AM-R
- Chromosome:
- 12q13.3
- Locus Type:
- gene with protein product
- Date approved:
- 2001-07-09
- Date modifiied:
- 2014-11-19
Related products to: GPR182 _ ADMR Rabbit antibody Ab Aff - Purified
Related articles to: GPR182 _ ADMR Rabbit antibody Ab Aff - Purified
- Familial adenomatous polyposis (FAP) is characterized by hundreds of colorectal adenomas that inevitably progress into carcinomas. This study focused on the heterogeneity during the polyposis progression to identify new targets and signatures for therapeutic development. - Source: PubMed
Publication date: 2026/03/27
Wu RuoyuLing YuhangHe YingYao LinhuaShi QianShen WeiyunLi XinboLiu YanLi Jingjing - The lymphatic system plays a central role in lipid absorption by transporting triglyceride-rich particles called chylomicrons (CMs) from the small intestine to the systemic circulation. However, the molecular mechanism by which CMs get into the intestinal lymphatics is unknown. Here we demonstrated that GPR182, an atypical chemokine receptor in lymphatic endothelial cells, mediates dietary fat absorption. GPR182 knockout mice exhibit a selective increase in circulating high-density lipoproteins and are resistant to dietary-induced obesity. GPR182 ablation in mice leads to poor lipid absorption and thereby a delay in growth during development. GPR182 broadly interacts with and transports lipoproteins. Transmission electron microscopy analysis reveals that mechanistically, loss of GPR182 prevents CMs from entering the lacteal lumen of the small intestine. Consistent with this, GPR182 blockade with monoclonal antibodies protects mice from diet- induced obesity and treats existing obesity. Together, our study identifies GPR182 as a lipoprotein receptor that mediates dietary fat absorption and supports GPR182 blockade as a feasible approach to treat obesity and related disorders. - Source: PubMed
Publication date: 2026/03/24
Sun ZhiweiTorphy Robert JMiller Emily NDarehshouri AnzaVigil IsaacTerai TaichiEleanor EckSun YiGuo YujieFykstra Dustin PYee Elliott JHu JunyiKedl Ross MLasda Erika LHesselberth Jay RSiegenthaler Julie AMacLean Paul SBruce Kimberley DRandolph Gwendalyn JSchulick Richard DZhu Yuwen - Angiogenesis is a critical process for tumor progression, regulated by various signaling pathways. Although antiangiogenic therapies targeting the VEGF pathway have shown potential, their effectiveness is inconsistent across different tumor types. GPR182, an endothelial cell-specific G protein-coupled receptor, is frequently downregulated in hypervascular tumors, but its specific role in angiogenesis has not been well defined. Our study reveals that GPR182 expression is markedly reduced in hepatocellular carcinoma (HCC) and inversely correlates with CD31, a pan-endothelial marker. In zebrafish embryos, Gpr182 deficiency resulted in enhanced angiogenic sprouting and hypervascularization, and GPR182-deficient human umbilical vein endothelial cells (HUVECs) showed increased migration and proliferation. At the molecular level, GPR182 acts as a decoy receptor, binding CXCL12 and regulating its gradient, which in turn suppresses CXCR4-mediated angiogenesis. The pharmacological blockade of CXCR4 with AMD3100 corrected the abnormal angiogenic phenotype in Gpr182-deficient zebrafish embryos and in the livers of a zebrafish HCC model. This work uncovers GPR182 as a negative regulator of angiogenesis, a key process in tumor growth and metastasis, and proposes that targeting GPR182 may offer a novel therapeutic approach for antiangiogenic strategies in cancer treatment. - Source: PubMed
Publication date: 2025/05/02
Chen ChangshengLiu WeiYuan FangWang XiaoningXu XiLing Chang ChunGe XiaojuanShen XiaozhongLi BowenShen YuqianLiu Dong - The unfolded protein response (UPR) is an adaptive and cytoprotective sensing-signaling network. Numerous studies have indicated the crucial role of UPR in the anti-tumor drug resistance and the modification of tumor microenvironment (TME). The aim of this study is to analyze the alterations of microenvironment and key regulatory genes in hepatocellular carcinoma (HCC) with high UPR activity. - Source: PubMed
Publication date: 2025/03/25
Wang YaoZhu Xiao FeiGu Wan JianZhang Gui Hong - The lymphatic system plays a central role in lipid absorption, which transports chylomicrons from the small intestine to the circulation. However, the molecular mechanism by which chylomicrons get into the intestinal lymphatics is unknown. Here we demonstrated that GPR182, a receptor in lymphatic endothelial cells (LECs), mediates dietary fat absorption. GPR182 knockout mice are resistant to dietary-induced obesity. GPR182 ablation in mice leads to poor lipid absorption and thereby a delay in growth during development. GPR182 binds and endocytoses lipoproteins broadly. Mechanistically, loss of GPR182 prevents chylomicrons from entering the lacteal lumen of the small intestine. GPR182 blockage with a monoclonal antibody (mAb) protects mice from dietary induced obesity. Together, our study identifies GPR182 as a lipoprotein receptor that mediates dietary fat absorption. - Source: PubMed
Publication date: 2025/02/07
Sun ZhiweiTorphy Robert JMiller Emily NDarehshouri AnzaVigil IsaacTerai TaichiEck EleanorSun YiGuo YujieYee Elliott JHu JunyiKedl Ross MLasda Erika LHesselberth Jay RMacLean PaulBruce Kimberley DRandolph Gwendalyn JSchulick Richard DZhu Yuwen