GPR182 Antibody (OALA00775)
- Known as:
- GPR182 Antibody (OALA00775)
- Catalog number:
- oala00775
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- GPR182 Antibody (OALA00775)
Related genes to: GPR182 Antibody (OALA00775)
- 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 Antibody (OALA00775)
Related articles to: GPR182 Antibody (OALA00775)
- The -adrenergic receptor, encoded by , couples to heterotrimeric G proteins, promoting intracellular calcium mobilization and PKC activation. In human hepatocytes, it regulates acute metabolic responses and impacts gene expression. Although fundamental hepatic functions of have been described, its role in hepatocellular carcinoma remains elusive. We hypothesized that expressed in liver cancer tissue is part of a signaling repertoire potentially linked to patient outcomes. We analyzed The Cancer Genome Atlas liver cancer datasets and found gene deletion in 6% of patients and more prolonged survival of patients with high expression. Thus, we aimed to identify -signaling partners equally linked to more prolonged patient survival. Through a rational data mining strategy, based on the identification of the signaling repertoire linked to expression and statistical correlation with patient survival, we identified a transcriptional signature integrated by the adrenoceptor and five candidate signaling companions including two RhoGEFs: and , a phospholipid phosphatase: , a RabGAP: , and an RTK adaptor: . Additionally, highly co-expressed GPCRs such as , , , , , and , and RTKs like and similarly integrated transcriptional signatures with that correlated with more prolonged survival. Most candidate signaling partners were well-co-expressed with hepatocyte markers, suggesting that integrating -associated signaling networks could improve liver cancer patients' prognosis. - Source: PubMed
Publication date: 2026/07/31
Beltrán-Navarro Yarely MabellVázquez-Prado JoséReyes-Cruz GuadalupeGarcía-Sáinz Jesús Adolfo - Excessive proliferation of crypt stem cells represents a crucial hallmark in colorectal tumorigenesis. G protein-coupled receptor 182 (GPR182), a recently partially "deorphanized" G protein-coupled receptor (GPCR), has emerged as a pivotal modulator in gastrointestinal tumors. However, its roles and underlying mechanism in colorectal tumors remain unclear, primarily due to the absence of identified endogenous ligands. In this study, we identified Insulin like growth factor binding protein 5 (IGFBP5) as a novel endogenous ligand for GPR182. GPR182 mRNA and protein expression levels were significantly up-regulated in cancer stem cells of colorectal tissues or cell lines. Functional assays revealed that IGFBP5 inhibited growth of intestinal crypt organoids and cancer stem cell spheres. In APC mice, IGFBP5 administration attenuated the tumor development while co-administration of GPR182 knockdown adeno-associated virus (AAV) abrogated this phenotype. Consistently, systemic IGFBP5 knockout markedly accelerated tumorigenesis and shortened survival time in APC mice. Mechanistic investigations demonstrated that IGFBP5's engagement with GPR182 induced inhibition of AKT/P70S6K pathway via Protein kinase C alpha (PKCα) dephosphorylation. Together, these findings elucidate the suppressive role of IGFBP5 in colorectal cancer (CRC) stem cells via GPR182/PKCα/AKT/P70S6K axis, highlighting IGFBP5 implementation a promising strategy for CRC. - Source: PubMed
Publication date: 2026/07/07
He YingRen Yuan-JiaLi Xin-BoZhou Yi-TongShi QianLiu YanShen WeiyunZhang Xi-LinWu Kang-ZhongLi Jing-JingLing Yu-HangTang Cheng-WuWang Xiang - 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