Mouse Monoclonal to Mouse PAI1 1mg
- Known as:
- Mouse Monoclonal Mouse PAI1 1mg
- Catalog number:
- IH34G6-1mg
- Product Quantity:
- 1mg
- Category:
- -
- Supplier:
- Innovative
- Gene target:
- Mouse Monoclonal PAI1 1mg
Related genes to: Mouse Monoclonal to Mouse PAI1 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: Mouse Monoclonal to Mouse PAI1 1mg
Related articles to: Mouse Monoclonal to Mouse PAI1 1mg
- The pathological mechanism of post-intracerebral hemorrhage (ICH) brain injury remains incompletely clarified. This study aims to clarify the role and molecular mechanism of miR-642b-3p in ICH, thereby providing a potential candidate target for clinical treatment. - Source: PubMed
Publication date: 2026/09/04
Rao ZhijuanLi Jiarong - Glutamic-Pyruvic Transaminase 2 (GPT2) significantly contributes to the advancement of colorectal cancer (CRC). This study aimed to elucidate the expression patterns, functional significance, and underlying mechanisms of GPT2 in CRC. Data from the TCGA repository, supplemented by immunohistochemical analysis, showed that GPT2 is substantially overexpressed in CRC specimens relative to adjacent non-cancerous tissues. This elevated expression level was further correlated with poorer clinical prognosis in patients. Cellular investigations using qPCR and Western blotting revealed differential GPT2 expression across CRC cell lines, with notably high levels in SW620 cells and minimal expression in SW1417 cells. Functional assays revealed that GPT2 overexpression in SW1417 cells notably increased their proliferation, migration, and invasion, while extending the G0/G1 cell cycle phase. Conversely, knocking down GPT2 in SW620 cells suppressed these malignant phenotypes and induced G2/M phase arrest. To investigate the molecular basis, RNA sequencing was performed on GPT2-knockdown SW620 cells, identifying 1020 differentially expressed genes. Enrichment analyses based on GO and the KEGG indicated that the identified genes are predominantly associated with biological processes related to the regulation of blood coagulation and functions localized within the endoplasmic reticulum lumen. Analysis of the PPI network for differentially expressed genes identified five core candidate genes: SERPINE1, CDKN1A, GADD45A, EPHA2, and ASNS. qPCR confirmed the expression levels of these genes, demonstrating a positive correlation with GPT2 expression. In conclusion, GPT2 acts as an oncogenic driver in colorectal cancer, enhancing tumor cell proliferation, migration, and invasive capabilities. This effect is likely mediated through the regulation of downstream targets, including SERPINE1 and CDKN1A. These findings suggest that GPT2 holds potential as both a prognostic indicator and a therapeutic target in colorectal cancer. - Source: PubMed
Publication date: 2026/08/28
Xu XiulianXie PingGan HailinHuang YimingLiu ZhihengLv Qijun - Congenital bronchopleural fistula is an exceptionally rare cause of persistent neonatal air leakage. Most bronchopleural fistulas in newborns are related to mechanical ventilation, infection, or iatrogenic injury. The clinical presentation can suggest pneumothorax commonly seen in premature infants, diagnosis is often delayed, and an ongoing uncontrolled air leak may significantly compromise effective ventilation. - Source: PubMed
Publication date: 2026/08/19
Janowicz TomaszSzostawicki Michał - 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
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