PTGES Antibody (N_term)
- Known as:
- PTGES Antibody (N_term)
- Catalog number:
- AP8589a
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- PTGES Antibody (N_term)
Related genes to: PTGES Antibody (N_term)
- Gene:
- PTGES NIH gene
- Name:
- prostaglandin E synthase
- Previous symbol:
- MGST1L1
- Synonyms:
- MGST-IV, PIG12, MGST1-L1, TP53I12
- Chromosome:
- 9q34.11
- Locus Type:
- gene with protein product
- Date approved:
- 1999-05-06
- Date modifiied:
- 2016-10-05
Related products to: PTGES Antibody (N_term)
Related articles to: PTGES Antibody (N_term)
- The bladder is highly susceptible to chemical carcinogens rendering bladder cancer one of the most prevalent cancers globally. While microsomal prostaglandin E synthase-1 (mPGES-1) is known to promote carcinogenesis in several tissues such as the colon and skin, its involvement in bladder cancer has not been fully investigated. This study aimed to clarify whether mPGES-1 promotes chemically-induced bladder carcinogenesis using a gene-deficient mouse model and evaluate its potential as a novel therapeutic target. - Source: PubMed
Sasaki YukaEndo YukiOchiai TsubasaKin MasaokiSuzuki YasutomoKondo YukihiroHara Shuntaro - Ovarian cancer shows limited responsiveness to immune checkpoint blockade, suggesting that malignant cells harbor intrinsic programs capable of suppressing T cell-mediated antitumor immunity. To uncover these programs under fixed recognition signal conditions, the research team established and optimized a B7H3×CD3-based, MHC-independent redirected cytotoxicity platform, which generated a reproducible partial-killing window. By screening 1796 bioactive compounds in paired SKOV3 monocultures and SKOV3/PBMC co-cultures, the researchers distinguished immune-sensitizing perturbations from direct cytotoxic agents and identified I-BRD9, a selective BRD9 bromodomain inhibitor, as a top candidate. I-BRD9 enhanced T cell-mediated killing in ovarian cancer models, B7-H3-positive benchmark cell lines, and patient-derived ovarian tumor suspensions, without affecting tumor cell or PBMC viability. Cross-cell line RNA-seq analysis revealed that BRD9 inhibition reshapes a coordinated immune resistance program involving PGE2 biosynthesis, inhibitory ligands, T cell-attracting chemokines, antigen presentation-related transcripts, and extracellular matrix features. Within this program, siRNA-mediated PTGES knockdown functionally recapitulated key effects of I-BRD9 by restoring chemokine/PGE2-axis transcripts, promoting CD8 T-cell proliferation and IFN-γ production, and enhancing T-cell effector-associated gene expression. These findings establish the BRD9-PTGES/PGE2 axis as an actionable tumor-intrinsic pathway that limits ovarian cancer sensitivity to T cell-mediated cytotoxicity. - Source: PubMed
Publication date: 2026/06/23
Guo ShanniShi PengYang ChangruiQian ShuyiYang FanYin XiaSun Bowen - Cerebral malaria (CM) is a life-threatening neurological complication of infection characterized by excessive inflammation, blood-brain barrier (BBB) disruption, and immune dysregulation. Macrophage-mediated inflammatory responses play a central role in CM pathogenesis, where imbalanced activation contributes to disease progression and tissue damage. However, integrated analyses combining macrophage surface phenotyping with transcriptional profiling remain limited, restricting comprehensive understanding of immune modulation during CM. - Source: PubMed
Publication date: 2026/06/10
Gupta AartiSharan Thakur RevaOjha Rajesh KumarKhan TahseenKalkal MeenuDas Jyoti - Uncontrolled hemorrhage in trauma, surgical, organ-related, and endoscopic settings, particularly in patients receiving antiplatelet therapy, remains difficult to manage clinically. Here, we introduce a high phosphatidylserine (PS)-exposed procoagulant platelet (hPPL) derivative reprogrammed from isolated platelets via calcium ionophore A23187-induced apoptosis, enriched in surface PS and capable of driving rapid hemostasis. Retaining a protein profile akin to resting platelets, hPPLs robustly promoted platelet activation and aggregation in human- and rat-derived plasma and whole blood in vitro and demonstrated superior hemostatic efficacy compared with clinical thrombin and commercial hemostatic materials [microporous polysaccharide hemispheres (MPH) and FIBRILLAR] in murine liver injury and porcine gastric ulcer bleeding models, even under antiplatelet treatment. Mechanistically, hPPLs up-regulated prostaglandin E synthase (PTGES), thereby increasing prostaglandin E2 (PGE) production and its receptor 3 (EP3)-mediated platelet activation, which reinforced PS-mediated clot formation. Our findings identified an apoptosis-driven PTGES-PGE-EP3 signaling axis that augmented PS-mediated coagulation in murine and porcine hemorrhage models and established the hPPL derivative as a topical hemostatic agent with translational potential for organ-related bleeding and distinct advantages in managing complex endoscopic hemorrhages under both physiological and coagulopathic conditions. - Source: PubMed
Publication date: 2026/06/03
Wang PeinaDu ShuailunWu SuyingZhai YaqiBai JiaweiSafdar AmmaraLiu ZhenyuLu ZefangLi BozhaoCheng JinSong YuchangZhang RuiLi DandanWang ZhichengZeng ZexianNie GuangjunChang Yan-ZhongLi Suping - Platelet-rich fibrin (PRF) is extensively utilized to enhance localized tissue healing, a process that critically depends on the transient polarization of macrophages toward a pro-inflammatory phenotype. Given that PRF, like other blood clot derivatives, may intrinsically modulate macrophage behavior, we conducted a comprehensive screening assay to characterize the global macrophage response to PRF exposure. To this end, we employed two widely used monocytic cell lines-U937 (histiocytic lymphoma) and THP-1 (acute monocytic leukemia)-as models to investigate macrophage responses. Cells were exposed to lysates derived from PRF, and transcriptomic alterations were profiled using bulk RNA sequencing. Differential gene expression analysis was performed, with significance determined by an adjusted p-value threshold of <0.05. In U937-derived macrophages, gene expression profiling revealed a transcriptional signature consistent with inflammatory activation. Clustering of upregulated genes highlighted pathways associated with chemokine activity (e.g., CCL2, CCL3, CCL4, CCL5, CCL7, CCL8, CCL20, CCL23, CCL26, CXCL5, CXCL6, CXCL8, CXCL16, and PPBP), RAGE receptor binding (FPR1, S100A8, S100A9, and S100A12), IgG binding (FCGR1A, FCGR2A, FCGR2B, and FCGR3A), prostaglandin biosynthesis (CBR1, CD74, EDN1, FABP5, IL1B, MIF, PTGES, and PTGS1), and collagen catabolism (CTSL, FAP, MMP3, MMP7, MMP9, MMP12, MMP14, MMP19, and MRC2). In contrast, PRF exposure in THP-1 cells primarily enriched genes involved in steroid biosynthesis, suggesting a more limited or distinct response. These findings underscore U937 cells as a more responsive and appropriate bioassay for modeling inflammatory macrophage polarization in response to PRF. Moreover, the identified gene signatures recapitulate key aspects of early wound healing, providing a relevant platform for studying macrophage reactivation in chronic wound environments. - Source: PubMed
Publication date: 2026/04/22
Panahipour LaylaHuang XiaoyuZampino FrancescaMiron Richard JGruber Reinhard