Human PAI1 uPA complex 0.1mg
- Known as:
- Human PAI1 uPA aggregate 0.1mg
- Catalog number:
- ICPAI-UPA-0.1mg
- Product Quantity:
- 0.1mg
- Category:
- -
- Supplier:
- Innovative
- Gene target:
- Human PAI1 uPA complex 0.1mg
Related genes to: Human PAI1 uPA complex 0.1mg
- Gene:
- SERPINE1 NIH gene
- Name:
- serpin family E member 1
- Previous symbol:
- PLANH1, PAI1
- Synonyms:
- PAI
- Chromosome:
- 7q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2019-04-23
Related products to: Human PAI1 uPA complex 0.1mg
Related articles to: Human PAI1 uPA complex 0.1mg
- Cancer-associated thrombosis (CAT) is a major cause of morbidity and mortality in patients with malignancy. Biomarkers of hypercoagulability and thromboinflammation may improve risk stratification and support personalised thromboprophylaxis, but evidence remains heterogeneous, particularly in cervical cancer. A systematic review was conducted according to PRISMA 2020. PubMed/MEDLINE, Scopus, Embase, and Web of Science were searched for studies published between January 2009 and March 2025 evaluating biological, molecular, genetic, and imaging biomarkers associated with hypercoagulability and thromboinflammation in women withcervical cancer. Evidence from breast cancer and broader CAT studies was incorporated to provide translational context. Owing to substantial methodological heterogeneity, findings were synthesised qualitatively. Twenty-five cervical cancer studies met eligibility criteria. D-dimer was the most extensively investigated biomarker and was consistently associated with VTE risk, although specificity was limited. Biomarkers of thrombin generation and fibrinolytic activation, including thrombin-antithrombin complexes, prothrombin fragment 1+2, and plasmin-α2-antiplasmin complex, demonstrated greater mechanistic specificity. Multimarker panels integrating coagulation, fibrinolysis, endothelial injury, platelet activation, and inflammation showed superior predictive performance compared with single biomarkers. Emerging biomarkers, including circulating tumour DNA, extracellular vesicles, and microRNAs, further supported tumour-driven thromboinflammation. SERPINE1 and F2 gene variants were associated with thrombotic risk and adverse prognosis. Current evidence supports further evaluation of integrated multimodal biomarker strategies for CAT risk assessment, but prospective, standardised, tumour-specific studies are required before biomarker-guided approaches can be implemented in clinical practice. - Source: PubMed
Publication date: 2026/08/16
Taizhanova DanaSerikbay NurgulCasas Pedro Henrique Fernandes do Carmo LasMijucic JovanaRoza BodaubayZubkov DmitryToleubekova DianaBovt VeronicaTazi Mezalek ZoubidaVandreden PatrickBaghdadi Mohammed ASaleem NidaTafur AlfonsoLefkou Eleftheria ElminaSiddiqui FakihaKempaiah PrakashaFareed JawedBitsadze VictoriaGerotziafas Grigoris T - : Oxidative stress is a major cause of RBC membrane damage, especially in individuals with G6PD deficiency who have impaired antioxidant defenses. Triphala, a phenolic-rich herbal formulation with known antioxidant activity, was evaluated for its phytochemical profile, antioxidant and anti-hemolytic effects, and molecular mechanisms in HO-induced oxidative stress models using normal and G6PD-deficient human RBCs. : Triphala aqueous extract was characterized using LC-MS and GC-MS. Antioxidant activity was evaluated by DPPH and ABTS assays. Cytotoxicity, membrane stability, and protection against HO-induced hemolysis were assessed in normal and G6PD-deficient RBCs. Network pharmacology, molecular docking and MD simulation analyses were performed to predict antioxidant-related mechanisms. Statistical analysis was conducted using one-way ANOVA ( < 0.05). : LC-MS identified gallic acid as the predominant phenolic compound, while GC-MS revealed pyrogallol as the major constituent. The extract showed strong radical scavenging activity and significantly reduced HO-induced hemolysis in both normal and G6PD-deficient RBCs without cytotoxicity ( < 0.05). Network pharmacology revealed that G6PD-related antioxidant regulation, oxidative stress response, and inflammatory signaling pathways are the key enriched biological processes. Network pharmacology analysis ranked PPARG, PTGS2, EGFR, MMP9, TLR4, ACE, REN, PPARA, SERPINE1, and MMP2 as the top hub proteins, highlighting their central roles in oxidative stress, inflammation, and metabolic signaling pathways. Kynurenic acid binds strongly to PTGS2 (COX-2) and ACE with binding affinities below -7.0 kcal/mol, forming multiple hydrogen bonds that stabilize its interactions within the active sites. MD simulations confirmed that kynurenic acid binds stably to ACE and PTGS2, with RMSD values plateauing near 2.4 Å and 3.0 Å, RMSF values mostly below 2 Å, and recurrent hydrogen bonding and electrostatic contacts with key residues, collectively underscoring its conformational stability, adaptive flexibility, and modulatory potential. : Triphala aqueous extract exhibits potent antioxidant and anti-hemolytic activities and may serve as a natural adjunct strategy for reducing oxidative damage in G6PD deficiency and related RBC disorders. - Source: PubMed
Publication date: 2026/08/19
Tedasen AmanRanjuanjit SiriwimonSrirod NattachaBunluepuech KingkanPereira Maria de LourdesNissapatorn VeeranootRattanawan ChutimaSangphech NaunpunBoonhok RachasakSarakul Orawan - Choroidal neovascularization (CNV) is a common and serious complication in various retinal diseases that involves the growth of new blood vessels from the choroid into the subretinal space, leading to a visual threat. Its underlying mechanism has not been fully uncovered. Discovering new genes related to CNV is an important way to reveal its molecular mechanisms. In this study, we used DisGeNET as the initial data source to identify genes related to CNV. The gene cluster method and additional screening tests were designed to explore the genetic landscape related to CNV. Our comprehensive analysis revealed many genes with high confidence, specifically identifying novel candidates that traditional topological methods missed. Notably, we identified SERPINE1, COL1A1, and ANGPT1 as unique gene signatures using our network embedding approach. Functionally, SERPINE1 regulates the plasminogen activation system to control proteolytic balance, COL1A1 maintains the structural integrity of the extracellular matrix during invasion, and ANGPT1 is critical for the maturation and stabilization of nascent vessels. Meanwhile, some genes were also identified by other methods, such as MMP2, a regulator of extracellular matrix degradation. The newly found genes are essential for understanding the process that initiates CNV. - Source: PubMed
Publication date: 2026/07/30
Liu LihuaZhang YuhangHuang FeimingBao YushengZhang Jian - Jing Guan Fang (JGF) is a traditional multi-herb formula used for hyperinflammatory conditions associated with severe viral infections; however, its protein-level effects in macrophage-mediated inflammation remain incompletely characterised. In this study, we combined ultra-performance liquid chromatography-quadrupole time-of-flight mass spectrometry (UPLC-QTOF-MS)-based phytochemical profiling, functional anti-inflammatory assays, and discovery-level proteomic and secretome analyses to investigate the anti-inflammatory effects of JGF in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages. Phytochemical profiling revealed predominantly flavonoid- and phenolic-related annotated features, together with selected terpenoid- and alkaloid-related annotations. Functionally, JGF treatment was associated with reduced nitric oxide production and differential effects on pro-inflammatory cytokine release, with a clearer concentration-dependent reduction in interleukin-6 (IL-6) and a more variable tumour necrosis factor-α (TNF-α) response, without reducing cell viability. Label-free quantitative proteomics suggested that JGF treatment was associated with modulation of LPS-induced protein changes, including reduced abundance of inflammation-associated proteins such as myristoylated alanine-rich C-kinase substrate (MARCKS) and inducible nitric oxide synthase (NOS2), together with partial restoration of selected regulatory proteins such as AIMP1 and AIMP2. Secretome analysis further suggested that JGF reduced extracellular inflammatory and tissue-remodelling-related mediators, including SERPINE1/PAI-1. Exploratory pathway analysis indicated that JGF treatment was associated with changes in inflammation-related and oxidative stress-related signalling networks. Collectively, these findings provide discovery-level molecular insights into the anti-inflammatory effects of JGF in LPS-stimulated macrophages and support further targeted validation of its pharmacological activity as a candidate multi-component anti-inflammatory formula. - Source: PubMed
Publication date: 2026/08/13
Yeon SeungyeonAlsherbiny Muhammad ASun Yu-TingLow Mitchell NLi Chun Guang - Hypoxia is a critical determinant in the etiology and progression of ischemic heart failure, but its underlying molecular mechanisms and regulatory interactions remain largely enigmatic. in our study, we employed differential analysis, coupled with WGCNA and the MSigDB database, to identify nine genes associated with hypoxia in heart failure. GO and KEGG enrichment analyses indicated that these genes are predominantly involved in hypoxia, immune responses, inflammation, apoptosis, and aging processes.Employing Bayesian networks, we elucidated four regulatory relationships among the hypoxia genes: PIM1-CDKN1A, IL6-CDKN1A, PLIN2-ANGPTL4, and SERPINE1-PLAUR. We amalgamated 12 machine learning algorithms, comprising 113 distinct combinations, to refine our findings and identified four pivotal hypoxia genes: SLC2A1, PLIN2, FOSL2, and PIM1. The SHAP analysis was instrumental in interpreting the predictive outcomes of the optimal model, the Random Forest algorithm, SLC2A1 was the most influential gene in the model. Immune infiltration analysis revealed the presence of seven types of dysregulated immune cells within the failing myocardium. Colocalization analysis showed that the posterior probabilities were predominantly concentrated on the gene-expression-only hypothesis and did not provide sufficient evidence for shared causal variants between the candidate-gene eQTL and HF GWAS signals. Overall, our research offers significant insights into the molecular mechanisms of hypoxia genes in the pathophysiology of heart failure, paving the way for the development of targeted and immunomodulatory therapies. - Source: PubMed
Publication date: 2026/08/26
Han QuanchengFan RuiqiMa JingjingYuan HuajingGuo YonghongXue YitaoYu YidingLi Yan