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
- Signal transducer and activator of transcription 5 (STAT5) is a key transcriptional regulator acting downstream of hematopoietic cytokines and hormones, such as erythropoietin (Epo), thrombopoietin or prolactin. STAT5-mediated gene regulation involves tyrosine phosphorylation at cytokine receptors and subsequent nuclear import. We studied STAT5 nucleocytoplasmic shuttling via live-cell imaging of fluorescent mutants in STAT5 HeLa EpoR cells. Unexpectedly, STAT5 mutants lacking the transactivation domain (TAD) were retained in the cytoplasm following Epo stimulation. Building upon this, we identified a 12-amino-acid stretch in the TAD sufficient to restore nuclear translocation. Further analysis revealed two residues within this 12‑amino‑acid stretch, D754 and D758, to be essential for nuclear import of phosphorylated full-length STAT5. Importantly, a single intact TAD in the STAT5 dimer is sufficient for nuclear import. Our findings reveal a unique role of the TAD in STAT5 nuclear trafficking distinct from other STATs, providing new mechanistic insight and potential targets for therapeutic intervention in STAT5-driven disease such as myeloproliferative neoplasms and leukemia. - Source: PubMed
Publication date: 2026/09/26
Ernst SabrinaBorgen-Möller MerithKüster AndreaSchurse HenningMüller-Newen Gerhard - Erythropoietin (EPO) is a hypoxia-responsive glycoprotein hormone that sustains erythroid progenitor survival through the erythropoietin receptor (EPOR). Beyond erythropoiesis, emerging evidence places the EPO/EPOR axis at the interface of tumor adaptation, stromal remodeling, and immune tolerance. Interpretation has been complicated by nonspecific antibodies, low receptor abundance, and failure to distinguish EPOR transcripts or intracellular proteins from ligand-accessible, functional cell-surface receptors. Recent mechanistic studies have established immunoregulatory roles: tumor-derived EPO reprograms EPOR-positive macrophages through nuclear factor erythroid 2-related factor 2 (NRF2)-dependent heme depletion, whereas EPOR signaling in conventional type 1 dendritic cells promotes tolerance and restrains antitumor T-cell priming. EPO-driven expansion of CD71-positive nucleated erythroid cells provides an additional systemic suppressive route. Evidence for direct effects on tumor cell survival, angiogenesis, and treatment resistance is more heterogeneous and must be interpreted in light of receptor validation, model context, and exposure conditions. This critical narrative review introduces operational evidence categories, distinguishes exploratory tissue screening from causal validation, and proposes a scalable experimental framework with minimum, enhanced, and gold-standard levels. Clinically, erythropoiesis-stimulating agents remain supportive care agents, not anticancer therapies; their use is restricted by thromboembolic risk and historical survival concerns. Translational development should prioritize practical biomarker panels and tumor- or cell-selective interventions that preserve erythropoietic safety. - Source: PubMed
Publication date: 2026/09/17
Yang TongshengZheng LinxingLan Tian - Cervical cancer represents a global public health problem, hence the importance of optimizing therapeutic options and expanding knowledge of prognostic markers. Clinical and experimental evidence shows that hypoxia-inducible factor (HIF) is a key inducer of aggressive phenotypes in cervical cancer: promoting angiogenesis, invasion, epithelial-mesenchymal transition (EMT), modulation of the immune microenvironment, and contributing to resistance to radiotherapy/chemotherapy in a possible synergistic effect with the human papilloma virus oncogenes. Hypoxic microenvironments that modulate the early activation of HIF pathways may be present in pre-invasive lesions and favor the acquisition of invasive phenotypes that precede invasion. This review highlights the mechanisms of HIF-1α in the progression of cervical intraepithelial neoplasia and cervical cancer. In this regard, HIF-1α is involved in the expression of genes related to angiogenesis, apoptosis and progression such as GLUT1, uPAR, BIRC5, EPO, EpoR, LIMD1, VHL, MET and pro-angiogenic genes (VEGF, PGF, PDGF-β, PAI-1, MMP-2, MMP-9, ANG-1, ANG-2, using pathways such as YAP/TA2. However, the balance between antitumor factors (miR-143) and protumor factors can define the progression of this neoplasia. In the future, the characterization of hypoxia signatures and the evaluation of HIF-1α pathway inhibitors are promising tools for optimizing outcomes in the treatment of cervical cancer, integrated with modern, high-precision radiation therapy techniques and predictive models based on imaging and artificial intelligence, which represent a key pillar of personalized oncology in cervical cancer, with the potential to improve tumor control and reduce toxicity; however, specific clinical trials are still needed to validate their impact on survival and safety. - Source: PubMed
Publication date: 2026/09/10
Carrero Yenddy NMosquera Jesús A - In vivo hematopoietic stem/progenitor cell (HSPC) gene therapy remains limited by low gene-editing efficiency and a lack of clinically applicable selection strategies to enrich therapeutically corrected progeny. We used in vivo base and prime editing to introduce a nonpathogenic EPOR variant into HSPCs, conferring erythropoietin hypersensitivity and promoting preferential expansion of gene-corrected erythroid cells. EPOR editing was combined with three therapeutic approaches for the correction of hemoglobinopathies: γ-globin gene addition, γ-globin reactivation, or correction of the sickle cell disease mutation. Tropism-modified helper-dependent adenoviral vectors (HDAd6/3+) targeting HSPCs were used to simultaneously deliver the EPOR-editing machinery and the corresponding therapeutic components. In vitro studies in an erythroid progenitor cell line and primary CD34+ cells demonstrated that the EPORW439* variant conferred a strong proliferative advantage to therapeutically modified erythroid progenitors. Mice humanized with CD34+ cells from a β⁰/β⁰-thalassemia patient were subjected to EPORW439*-mediated EPO hypersensitivity alongside a therapeutic γ-globin transgene which resulted in >70% HbF-positive erythroid cells and substantial reversion of the disease-associated phenotype, including reduced oxidative stress, near-complete elimination of splenic iron deposition, and reduced splenomegaly. Importantly, these effects were achieved after simple intravenous administration of the vectors following HSPC mobilization and cytokine prophylaxis, without subsequent pharmacologic selection. Together, these findings establish a strategy to amplify the therapeutic benefit of otherwise limited in vivo HSPC gene editing for hemoglobinopathies. - Source: PubMed
Publication date: 2026/09/17
Sakunthala Velmurugan AksharaPaschoudi KiriakiQueenan Jack AGil SucheolMaynard AidanFontana Charlie ESharma RevaLong AnikaLi ChangWang HongjieAnderson Anna KGeorgakopoulou AphroditePsatha NikolettaGiannaki MariaVlachaki EfthymiaAhmed NouraizSousa Alexander ALiu David RYannaki EvangeliaLieber AndreKaruppusamy Karthik V - The immune system balances protective immunity against pathogens with tolerance to self and selected foreign antigens. Emerging evidence identifies erythropoietin (EPO) as a systemic immunoregulatory signal that links physiological stress to immune adaptation. Beyond its canonical role in erythropoiesis, EPO-EPO receptor (EPOR) signaling reprograms specialized myeloid cells, including macrophages and type 1 conventional dendritic cells (cDC1s), promoting efferocytosis, inflammatory restraint, and maturation-associated cDC1 fate. Through these mechanisms, EPO shapes antigen-specific T-cell responses across transplantation and cancer. We propose that the EPO-EPOR axis functions as a systemic regulator of immune adaptation through myeloid-cellprogramming. - Source: PubMed
Publication date: 2026/09/16
Zhang XiangyueEngleman Edgar G