GPR182 siRNA_Lentivectors
- Known as:
- GPR182 siRNA_Lentivectors
- Catalog number:
- i009116c
- Product Quantity:
- 500ng
- Category:
- -
- Supplier:
- ABM
- Gene target:
- GPR182 siRNA_Lentivectors
Related genes to: GPR182 siRNA_Lentivectors
- 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 siRNA_Lentivectors
Related articles to: GPR182 siRNA_Lentivectors
- Historically, research on chylomicron entry into intestinal lymphatic vessels (lacteals) has been polarized between paracellular and transcellular transport models. In this issue of the JCI, Sun et al. identified GPR182 as a lipoprotein receptor in lymphatic endothelial cells (LECs), profoundly advancing our understanding of intestinal lipid absorption. They observed poor fat absorption in GPR182-deficient mice and demonstrated the role of GPR182 in transporting chylomicrons across the LECs into the lacteal lumen. This discovery establishes a molecular basis for transcellular transport of chylomicrons, challenging the traditional view that lacteal lipid entry is predominantly paracellular. By linking receptor-mediated uptake to impaired fat absorption and protection against fat-induced obesity and steatosis, this study expands the biological and translational implications of lacteal transport. Consequently, rather than favoring a single model, future research should investigate the integration of both paracellular and transcellular transport models in vivo. - Source: PubMed
Publication date: 2026/06/15
Yu Liqing - 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-KO mice exhibited a selective increase in circulating high-density lipoproteins and are resistant to diet-induced obesity. GPR182 ablation in mice led to poor lipid absorption and thereby a delay in growth during development. GPR182 broadly interacted with and transported lipoproteins. Transmission electron microscopy analysis revealed that, mechanistically, loss of GPR182 prevented CMs from entering the lacteal lumen of the small intestine. Consistent with this, GPR182 blockade with mAbs protected mice from diet-induced obesity and treated 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 treating obesity and related disorders. - Source: PubMed
Publication date: 2026/03/24
Sun ZhiweiTorphy Robert JMiller Emily NDarehshouri AnzaVigil IsaacTerai TaichiEck EleanorSun 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