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
- Asialoglycoprotein receptor 1 (ASGR1), a hepatocyte-specific receptor, represents a potential therapeutic target for hypercholesterolemia. However, liver safety risks of ASGR1-targeted therapies remain poorly characterized. This study aims to investigate the impact of ASGR1 deficency on liver fibrosis and its underlying mechanisms. - Source: PubMed
Zhu HuiHuang Xin-PingYou KaiChen YanLi Peng-HuiTao Jia-WangYu Xiao-RuiXu Jie-HuiXu Guo-ShengLi Yin-Xiong - Long-term patency of saphenous vein grafts (SVGs) remains a significant challenge in coronary artery bypass grafting (CABG). The biological factors underlying successful human grafts are poorly understood. We aimed to characterize the structural and molecular features associated with successful graft function. - Source: PubMed
Publication date: 2026/08/13
Kim Eun NaSohn Suk HoYu JiyoungLim Joon SeoKoh JiwonKoh JaemoonHwang ChanghaKim KyunggonHwang Ho YoungOh Se Jin - Non-small cell lung cancer (NSCLC) remains a leading cause of cancer-related mortality worldwide, with limited therapeutic efficacy due to tumor heterogeneity in conventional treatments. In the present study, an integrative, network pharmacology approach was employed to elucidate the multi-target mechanism of action of phytochemicals derived from Glossocardia bosvallia against NSCLC. Among 38 phytocompounds identified, 31 compounds that satisfied pharmacokinetic properties were selected for subsequent analysis. Ligand-based target prediction identified 429 potential protein targets, which are integrated with the top 250 differentially expressed genes obtained from the GSE33532 dataset. Intersection analysis identified eight therapeutic targets: PTGES, SRD5A1, CDK1, KIF11, TOP2A, CDC45, MB, and CHEK1. Protein-protein interaction and enrichment analyses demonstrated that these targets are predominantly involved in cell cycle regulation, mitotic cell cycle, and DNA replication pathways. Gene expression analysis demonstrated significant overexpression of the prioritized targets in NSCLC tissues, while survival analysis identified CHEK1 as the gene significantly associated with survival (p < 0.05). Molecular docking identified TOP2A_quinic acid as the most favorable complex, exhibiting a binding affinity of -12.27 kcal/mol, KIF11_linoleic acid as -12.10 kcal/mol and CHEK1_2,3-dihydro-3,5-dihydroxy-6-methyl-4h-pyran-4-one as -6.75 kcal/mol, which was further validated by dynamic simulations, principal component analysis based free energy landscape, and DSSP analysis, confirming the stability of the protein. This integrative framework provides a robust strategy for identifying biologically relevant and therapeutically actionable targets supporting the potential of G. bosvallia-derived phytochemicals as promising candidates for NSCLC. - Source: PubMed
Publication date: 2026/08/04
Kulandhaivel Soundar RajanStalin AntonyMuthuramalingam PandiyanSivaprakasam BalasubramanianJesudass Joseph Sahayarayan - Sepsis is a life-threatening organ dysfunction caused by a dysreg- ulated host response to infection, with the immune status dynamically evolving from an early hyperinflammatory phase to a late immunosuppressive phase. ABCA1 (ATP-binding cassette transporter A1) is involved in cholesterol efflux and inflammatory regulation, but its causal relationship with sepsis, cellular ori- gin, and potential for drug targeting remain unclear. This study is the first to integrate Mendelian randomisation, single-cell transcriptomics, in silico knock- out, and virtual screening to systematically investigate ABCA1 in sepsis from genetics, cell biology, mechanisms, and translational potential. - Source: PubMed
Publication date: 2026/08/07
Yu YangZhang Sheng - Colorectal cancer (CRC) is one of the global health issues. Current treatments still present major challenges such as off-target cytotoxicity and the emergence of drug resistance, the development of potent and innovative therapeutics is urgently needed. Here, we synthesized copper‑aluminum (CuAl) layered double hydroxides (LDH) using a hydrothermal method and loaded them with the 5-fluorouracil (5-FU) (CuAl-5FU) to improve their anticancer efficacy. The LDHs were 2D-sheeted and rosette-like in shape. The hydrodynamic diameter of CuAl and CuAl-5FU was 568 and 661 nm, respectively. Zeta potential values of CuAl-5FU ranged from +31.39 to +34.93 mV across pH 3 to 9, indicating good colloidal stability. The drug loading and encapsulation efficiency were 18.19% and 36.37%, respectively. Dose-dependent cytotoxicity was seen in HCT-116 and HT-29 CRC cells. Comparatively, CuAl-5FU LDH exhibited greater anticancer activity compared to LDH alone and free 5-FU drug in both monolayer and tumor spheroid models. Mechanistic studies revealed that CuAl-5FU significantly induced reactive oxygen species (ROS) production, mitochondrial membrane depolarization, and promoted apoptosis by upregulating the pro-apoptotic Bax protein and PARP cleavage in both CRC cells. Transcriptomic analysis and qPCR validation revealed the downregulation of oncogenic MAPK signaling and modulation of key genes related to proliferation (JUN, DUSP1, FOSB, EGR1, and FOS), apoptosis (TP53I3, ZMAT3, GADD45A, BBC3, MDM2, TNFRSF10B, E2F1, and ORC1), and cell cycle arrest (CDKN1A and CDC25A). Notably, we identified altered expression of several chemoresistance-related genes (AVPI1, HROB, DDIAS, PTGES, and LAMA3), suggesting the early emergence of adaptive responses in CRC cells. To validate this observation, CuAl-5FU-resistant HCT-116 G3 and HT-29 G2 cell lines were established and their chemoresistant phenotypes were characterized. Indeed, the chemoresistance-associated genes were upregulated, together with significantly higher IC values and clonogenic survival fractions than their respective parental cells. Collectively, these findings suggest that CuAl-5FU improves anticancer activity in CRC cells by modulating multiple genes involved in ROS production, mitochondrial membrane depolarization, apoptosis, and cell cycle regulation. Nevertheless, chemoresistance developed rapidly following repeated treatment, highlighting a potential limitation of this therapeutic approach. Overall, this study provides a new potential strategy for CRC treatment while emphasizing the importance of elucidating the molecular mechanisms underlying acquired chemoresistance. Future studies should also optimize the physicochemical properties of the CuAl-5FU LDH, particularly the large particle size (∼661 nm) by optimizing the hydrothermal synthesis conditions and incorporating surface modifications to further improve the tumor penetration and drug delivery. - Source: PubMed
Publication date: 2026/07/10
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