PTGES Antibody (N-term) Blocking Peptide
- Known as:
- PTGES Antibody (N-terminus) Blocking Peptide
- Catalog number:
- BP8589a
- Product Quantity:
- 2
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- PTGES Antibody (N-term) Blocking Peptide
Related genes to: PTGES Antibody (N-term) Blocking Peptide
- 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) Blocking Peptide
Related articles to: PTGES Antibody (N-term) Blocking Peptide
- 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 - The corpus luteum (CL) is essential for progesterone production and maintenance of early pregnancy in ruminants. Luteal function is critically influenced by the balance between prostaglandin E (PGE) and F (PGF), which is regulated by key synthases such as PTGES and PGFS. Interferon-tau (IFNT), the pregnancy recognition signal in ruminants, is known to modulate prostaglandin production. However, its precise role and underlying mechanisms in regulating PGE and PGF production within goat CL remain unclear. In this study, the expression of key prostaglandin synthases was progressively upregulated in the CL throughout early pregnancy (days 5-18), accompanied by an increase in the PTGES/PGFS ratio. In goat luteal cells, IFNT significantly increased PTGES expression without affecting PGFS, and elevated the PGE/PGF ratio. IFNT dose- and time-dependently induced ISG15 expression, and concurrently upregulated ISGylation-related enzymes. Notably, ISG15 overexpression recapitulated the effects of IFNT by selectively upregulating PTGES expression, thereby enhancing PGE production and the PGE/PGF ratio. Conversely, ISG15 knockdown attenuated the IFNT-induced effects. Further mechanistic investigations revealed that both conjugated and free forms of ISG15 contribute to the upregulation of PTGES and the subsequent increase in the PGE/PGF ratio. Collectively, these findings identify ISG15-mediated elevation of the PGE/PGF ratio as a key mechanism by which the pregnancy recognition signal IFNT protects the CL, providing new insights into the maintenance of early pregnancy in goats. - Source: PubMed
Publication date: 2026/04/21
Shang ChunmeiLiu HaokunLi ZuhuiMou YuanmengFan ChenlingLiu ShanJin YapingLin Pengfei - Diabetic kidney disease (DKD) is significantly impacting both quality of life and survival rates. The Shen-Yan-Fang-Shuai (SYFS) formula is a traditional Chinese medicine (TCM) compound widely used in the clinical treatment of DKD with proven efficacy, though its potential mechanism of action remains unclear. This study attempts to elucidate the therapeutic efficacy, mechanisms of action, and active compounds of the SYFS formula in the treatment of DKD. - Source: PubMed
Kang YiJin QianZhou MengqiZheng HuijuanLi DanwenWang XuezheZhou JingweiLv JieWang Yaoxian