Human PAI1 stable mutant form 1mg
- Known as:
- Human PAI1 stable mutant form 1mg
- Catalog number:
- ICPAI-1mg
- Product Quantity:
- 1mg
- Category:
- -
- Supplier:
- Innovative
- Gene target:
- Human PAI1 stable mutant form 1mg
Related genes to: Human PAI1 stable mutant form 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 stable mutant form 1mg
Related articles to: Human PAI1 stable mutant form 1mg
- Radiotherapy failure remains a major challenge in glioblastoma (GBM), yet the stress-adaptive programs that enable tumor cells to survive irradiation-induced lethal injury remain incompletely defined. This study investigated whether serpin family E member 1 () contributes to GBM radioresistance by modulating ferroptosis-associated lipid peroxidation, a process linked to iron-dependent oxidative injury. - Source: PubMed
Wang YuhangLi YantingDong MengZeng ChaoJin ZhuanmeiZhang QiuningYuan Wenzhen - High-altitude pulmonary edema (HAPE) is a severe complication of rapid exposure to high-altitude hypoxia, but its molecular mechanisms remain incompletely understood. This study aimed to characterize lung proteomic alterations in HAPE and identify candidate proteins associated with its pathophysiological processes. - Source: PubMed
Publication date: 2026/09/14
Zhang DongmeiLiu TingtingMu HongfangLi XiaolinYang ChenyuLi WenbinWang Rong - To reconnoitre the mechanism of Abietic acid (AA) in diabetes by and experiments. Using GeneCards, diabetes gene targets were obtained. The protein-protein interaction and network topology analysis were performed using the String platform and Cytoscape 3.7.2. The enrichment analysis was done by Shiny GO. The docking was by Autodeck. Diabetes was induced by injecting STZ (55 mg/kg, i.p once) in Sprague-Dawley rats. The parameters included glucose, lipids, blood pressure, ECG, OGTT, kidney and cardiac markers, liver enzymes, AMPK, Nrf2, PPAR-γ, TLR-4, oxidative markers, LVF tests, and histopathology. AA interacts with 15 important targets (PIK3CD, MAPK1, NF-κB, mTOR, STAT3, GRIN1, ITGB3, ACACA, HSP90AB1, SERPINE1, ADRB1, ULK1, TLR4, CTSD, CDK5). The signalling pathways, like insulin, MAPK1, TLR, AMPK, JAK-STAT, are associated with these proteins. In docking, the highest affinity of AA was observed for ITGB3 (- 8.1), TLR4 (- 7.8), and ACACA (- 7.3). In rats, AA(40 and 80 mg/kg) decrease hyperglycaemia and hyperinsulinemia, improves glucose tolerance, normalize blood pressure, combat dyslipidaemia (decrease triglyceride, total cholesterol, LDL, increase HDL), preserves myocytes and ventricular function (decrease troponin-I, LDH, CK-MB, LVEDP, normal ECG), hepatoprotective (decrease AST, ALT), reno-protective (decrease creatinine, urea, uric acid) and combat oxidative stress (decrease MDA, increase SOD, catalase). Nrf2, AMPK, and PPAR γ levels were increased while TLR-4 levels were decreased after AA treatment. The study is supported by the preserved histopathological architecture of pancreatic, renal, hepatic, and cardiac cells. The present study preliminarily clarifies that AA exhibits therapeutic potential in preclinical models through multitargets and multi-pathways (Nrf/TLR4/PPAR γ), which points out a new direction for further research and clinical application. - Source: PubMed
Publication date: 2026/09/24
Mishra AkashShah Hital - Gangrenous mastitis is a severe form of mastitis in dairy goats that causes extensive tissue damage and has a poor prognosis, thereby substantially affecting the dairy goat industry; however, its molecular pathogenesis remains unclear. In this study, was used to establish a model of gangrenous mastitis in dairy goats. Mammary gland tissues were collected at 72 h post-inoculation for transcriptomic and proteomic sequencing, followed by integrated multi-omics analyses to systematically identify key regulatory pathways and candidate molecules associated with -induced gangrenous mastitis. The results showed that clinical mastitis was characterized mainly by activation of pathways related to the acute inflammatory response, pathogen recognition, neutrophil chemotaxis, and phagocytic defense. In contrast, gangrenous mastitis involved broader molecular reprogramming, with significant enrichment of the TNF, IL-17, and NF-κB signaling pathways, complement and coagulation cascades, platelet activation, and extracellular matrix (ECM) remodeling. Protein-protein interaction (PPI) analysis, gene set enrichment analysis (GSEA), and validation of key molecules indicated that IL6, S100A8, THBS1, SERPINE1, and MMP9 may represent important nodes in disease progression. Collectively, these findings indicate that gangrenous mastitis is a complex infectious tissue-injury process driven by inflammatory amplification, aberrant immune-cell activation, complement-coagulation dysregulation, and tissue structural disruption. The identified molecules and pathways may facilitate the development of biomarker panels for early diagnosis and risk stratification and inform preventive and adjunctive therapeutic strategies targeting excessive inflammation, microcirculatory dysfunction, and ECM damage in dairy goats. - Source: PubMed
Publication date: 2026/09/12
Fu MingzheTan XuewenLiu YingqiuZhang WeiminZhuang ShenAn XiaopengFan Yunpeng - Plasminogen activator inhibitor 1 (PAI-1) is a key regulator of fibrinolysis, and its deficiency causes bleeding symptoms. PAI-1 deficiency is rare, and pathogenic variants are only sporadically reported. - Source: PubMed
Publication date: 2026/08/27
Haisma BaukeNieuwenstein ThomasRijpma Sanna RSimons AnnetBlijlevens Nicole M Avan Heerde Waander LSchols Saskia E M