Ask about this productRelated genes to: PTGER2 antibody
- Gene:
- PTGER2 NIH gene
- Name:
- prostaglandin E receptor 2
- Previous symbol:
- -
- Synonyms:
- EP2
- Chromosome:
- 14q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 1994-07-29
- Date modifiied:
- 2016-10-05
Related products to: PTGER2 antibody
Related articles to: PTGER2 antibody
- Muscle satellite cells are adult muscle stem cells indispensable for growth and regeneration of postnatal skeletal muscle. Notch plays a central role in maintenance of muscle satellite cells, but how Notch maintains the muscle stem cell pool is not fully understood. Previously, we reported that a prostaglandin E2 receptor, EP2, is upregulated by Notch signal and suppresses differentiation of human muscle progenitors. Here we examined the roles of EP2 in muscle satellite cells using a mouse Cre-LoxP conditional gene knockout system. Genetic inactivation of the EP2 gene (PTGER2) activated muscle satellite cells, caused their loss, and impaired muscle regeneration. These results indicate that EP2 is indispensable for maintenance of satellite cells. Ex vivo analysis using isolated myofibers showed that prostaglandin E2 (PGE2) delayed the activation of satellite cells via EP2. An extracellular signal-regulated kinase (ERK) 1/2 inhibitor blocked the activation of satellite cells on myofibers, and PGE2 attenuated the phosphorylation of ERK1/2 in muscle satellite cells. These results suggest that EP2 keeps the quiescence of satellite cells and maintains the satellite cell pool in part by inhibiting the ERK1/2 signaling pathway. - Source: PubMed
Maruyama YusukeNogami Ken'ichiroMotohashi NorioSakai-Takemura FusakoElhussieny AhmedUchiumi FumiakiAoki YoshitsuguTakeda Shin'ichiMiyagoe-Suzuki Yuko - Neutrophils have recently been demonstrated to play a variable role in cancer progression, likely due to adaptability to environmental signals that influence neutrophil phenotype and function. In the tumor microenvironment, tumor-derived prostaglandin E2 is well established as a major suppressor of immune cell function and facilitates tumor immune evasion. However, while prostaglandin E2 is widely regarded to signal through the E-prostanoid receptors type (EP) 2 and EP4 on neutrophils, the exact effects of targeting this axis therapeutically in the context of cancer remain largely unexplored. In this study, we investigated the effect of prostaglandin E2 signaling via EP2/4 in human neutrophils using specific EP2 and EP4 antagonists. We report that countering EP2/4 signaling yields an activated phenotype together with the acquisition of proinflammatory properties, including the augmented production of reactive oxygen species, enhanced phagocytosis, and increased production of IL-8. Given the phagocytic nature of neutrophils, we encapsulated EP2/4 antagonists into poly (lactic-co-glycolic acid) nanoparticles for the tailored delivery of these antagonists. Importantly, nanoparticles achieved robust phenotypical and functional activation of healthy neutrophils as well as cancer patient-derived neutrophils exposed to tumor-derived prostaglandin E2. Together, these results identify the role of EP2/4 in regulating activation of human neutrophils and illustrate the relevance of targeting this axis with nanoparticles in the context of cancer for the reactivation of tumor-exposed neutrophils. We propose that targeting this axis in neutrophils using nanoparticles can serve to attenuate tumor-induced suppression by steering them toward a proinflammatory state and thus potentially support antitumor immune responses. - Source: PubMed
Bödder JohannaKramer RobbinMinnee JuliaCuenca-Escalona JorgeBootsman SharonFauerbach JonathanFlórez-Grau Georginade Jong Esther Cde Vries Jolanda M - Glioblastoma (GBM) remains one of the most lethal brain tumors, characterized by extensive immune evasion and a macrophage-dominated tumor microenvironment (TME). However, the molecular determinants governing tumor-associated macrophage (TAM) states and their immunoregulatory functions remain poorly understood. We integrated bulk- and single-cell transcriptomic datasets (TCGA, CGGA, Ivy GAP, and Brain Immune Atlas) to systematically characterize the expression, prognostic relevance, and immune contexture of the myeloid biomarker membrane-spanning 4-domain A6A, , in GBM. Differential expression, survival, and pathway enrichment analyses were performed. Single-cell mapping and CellChat modeling delineated -associated TAM subpopulations, intercellular communication networks, and ligand-receptor signaling dynamics. Spatial transcriptomic validation and pharmacogenomic modeling were conducted to assess anatomic enrichment and therapeutic vulnerabilities. High expression predicted unfavorable survival and correlated with increased stromal and immune infiltration. Single-cell analyses localized predominantly to TAMs, especially Regulatory- and Ribo-TAM states enriched for antigen presentation, T-cell regulation, and ribosomal biogenesis pathways. CellChat analysis revealed that -high TAMs exhibited markedly enhanced communication with CD4 T cells and Tregs through upregulated PGE-PTGER2/PTGER4, PECAM1-CD38, and THBS1-CD36 signaling axes, implicating in prostaglandin-driven immune suppression. Spatial profiling confirmed preferential localization of within perivascular and angiogenic niches. Pharmacogenomic prediction indicated that -high tumors were more sensitive to ERK, mTOR, and CDK4/6 inhibition. defines a macrophage-centered, immunosuppressive ecosystem in GBM, mediated by the activation of the PGE signaling axis. These findings position both as a prognostic biomarker and as a potential therapeutic node linking myeloid reprogramming to actionable pathway vulnerabilities in glioblastoma. - Source: PubMed
Publication date: 2025/12/20
Chen JiananWu QiongBerglund Anders EMacaulay Robert JMulé James JEtame Arnold B - Human immunodeficiency virus (HIV) and (Mtb) co-infection remains a major cause of mortality in AIDS patients, yet the mechanisms of pathogen interplay and host immune remodeling remain poorly understood. - Source: PubMed
Publication date: 2025/11/28
Zhao ZihuiHuang SuyueHuang WeiSong WeiLiu LiChen JunZhang RenfangShen Yinzhong - Seasonal reproduction in mammals is primarily regulated by the hypothalamic-pituitary-ovarian (HPO) axis, yet its molecular mechanisms in subterranean rodents living in light-restricted environments remain poorly understood. This study aimed to characterize the transcriptional regulation of the HPO axis during seasonal estrus in the Manchurian zokor (, ), a fossorial rodent exhibiting distinct breeding cycles despite perpetual darkness. - Source: PubMed
Publication date: 2025/10/30
Nai RileLi XueruShan DanBao SaruWang FeiLin YuerongZhang YanHu BuqinXie YuchunMan Duhu