Ask about this productRelated genes to: EPOr antibody
- Gene:
- EPOR NIH gene
- Name:
- erythropoietin receptor
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 19p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1990-05-14
- Date modifiied:
- 2017-07-12
Related products to: EPOr antibody
Related articles to: EPOr antibody
- To explore the alterations in the microbiota and transcriptome of patients with chronic atrophic gastritis (CAG) and liver cirrhosis (LC) and to develop robust diagnostic models. - Source: PubMed
Publication date: 2026/08/21
Zhu YiqingZhang GuomingMa RuiguangLi QianDai HuayuLi ZhouyueLi LixiangLi Zhen - Congenital Dyserythropoietic Anemia type I (CDA-I) is an autosomal recessive disease characterized by anemia due to ineffective erythropoiesis and results primarily from mutations in CDAN1, which encodes CODANIN1. Research efforts to understand the CDA-I pathogenesis have been impeded by the embryonic lethality of germline Cdan1 deleted mice as well as mice deleted for Cdan1 in the erythroid compartment, using the constitutively active EpoR-Cre allele. To study the function of CODANIN1 in adult erythropoiesis, we generated mice with inducible erythroid-specific biallelic Cdan1 deletion using the Gata1-CreERT2 allele. Following tamoxifen administration to adult mice, Cdan1 is excised, resulting in features of CDA-I, including anemia, impaired erythroid differentiation, disturbances in erythroblast cell cycle progression, and the finding of 'spongy' heterochromatin in bone marrow erythroblasts. These findings confirm a critical role for CODANIN1 in effective adult erythropoiesis and demonstrate the successful generation of an inducible CDA-I mouse model, which serves as a valuable platform for testing novel therapies for this orphan disease. - Source: PubMed
Publication date: 2026/09/02
Friedman AnnKing Richard AMyers GreggoryYu LeiBergin Ingrid LLin ZesenDrysdale ClaireMullin CareaCruz Edgar DBalbin-Cuesta GinetteLiu Xiaofang LGallagher Patrick JZhu GuojingMcGee BethLang AnnemarieSingh Sharon AEngel James DouglasGallagher Patrick GKhoriaty Rami - We discovered that vitamin C import through the vitamin C transporter SLC23A2 in stress-specific erythroid progenitors represents a key regulatory nexus in the recovery of the erythron. In response to erythroid stress, such as blood loss, Epo induces the expression of Slc23a2 in stress erythroid progenitor cells, increasing intracellular vitamin C levels and promoting their differentiation into erythroblasts. Vitamin C-induced erythroid differentiation is blocked by Slc23a2 deletion or in EpoR mutant mice unable to induce Slc23a2. Both mice show attenuated erythron recovery in stress. These defects are rescued by exogenous expression of either SLC23A2 or the related vitamin C transporter SLC23A1, but not by a transport-defective SLC23A2 mutant. Mechanistically, intracellular vitamin C promotes erythroid progenitor differentiation independently of its antioxidant activity. Instead, it regulates 2-oxoglutarate-dependent dioxygenases, TET2, KDM6A and ALKBH8, facilitating the upregulation of the master erythroid transcription factor GATA1. These findings identify vitamin C uptake as an Epo-licensed, rate-limiting determinant of stress erythropoiesis. - Source: PubMed
Publication date: 2026/09/02
Hsieh Hsi-HsienMa YueDeVilbiss Andrew WComazzetto StefanoSubramaniyan IndhumathyJun Ji HyungVoit Richard ALi LiAgathocleous MichailHuang Lily Jun-Shen - Intravascular hemolysis is a hallmark of sickle cell disease (SCD). While it has been well established that the hemolysis-derived products, such as hemoglobin (Hb) and free heme, exert proinflammatory and pro-oxidative effects, contributing to the vascular and tissue damage in SCD, the effects of hemolysis on erythropoiesis have not been studied. We and others have reported that hemolysis in SCD led to upregulation of type I interferon IFNα. We further documented that the ability of Townes sickle mice to increase their erythropoietic capacity to compensate for anemia was impaired. To examine whether the impaired erythropoiesis in SCD is associated with the hemolysis-driven IFNα production and to define the underlying mechanisms, we injected mice with hemin, red cell lysate, or IFNα to mimic the hemolysis status in SCD and then examined erythropoiesis by colony-forming assay, flow cytometric analysis, and western blot. We also examined the effects of hemin and IFNα on erythropoiesis using an in vitro erythroid culture system. We found that intravascular hemolysis inhibited erythropoiesis in SCD through inhibition of erythropoietin (EPO)/erythropoietin receptor (EPOR) signaling via a heme-IFNα-CISH axis. Herein, we describe how to prepare hemin, red cell lysate, and IFNα, and present examples of in vivo and in vitro assays to assess erythropoiesis. Our methods can be applied to study changes in erythropoiesis in other diseases characterized by intravascular hemolysis. - Source: PubMed
Zhang HuanAn Xiuli - Erythropoiesis-targeted doping remains a major challenge for sports medicine because pharmacological and genetic manipulation of erythropoiesis can improve oxygen transport and endurance performance while increasing the risk of serious cardiovascular complications. Erythropoiesis-targeting strategies extend beyond recombinant erythropoietin (EPO) to include hypoxia-inducible factor prolyl hydroxylase inhibitors (HIF-PHIs), modified erythropoietin receptor (EPOR) agonists, transforming growth factor beta (TGF-β) signaling inhibitors, cytoprotective EPO derivatives, and gene- or cell-based approaches, and require complementary detection strategies based on direct analytical methods and the Athlete Biological Passport (ABP). Although they may enhance oxygen delivery and endurance performance, excessive stimulation of erythropoiesis may increase blood viscosity, impair vascular function, and elevate the risk of hypertension, thromboembolic complications, and other cardiovascular (CV) events. Erythropoiesis-targeted doping has evolved beyond recombinant EPO into a diverse group of pharmacological and genetic strategies that require increasingly sophisticated detection approaches. A thorough understanding of their molecular mechanisms and cardiovascular consequences is essential for improving anti-doping surveillance and protecting athlete health. This review summarizes current erythropoiesis-targeting agents, their mechanisms of action, detection strategies, cardiovascular risks, and implications for anti-doping practice. - Source: PubMed
Publication date: 2026/08/12
Chlebowska GabrielaMichalak KrzysztofMazur ŁukaszSzczurek-Wasilewicz Wioletta