PAI1 antibody
- Known as:
- PAI1 (anti-)
- Catalog number:
- 10-1939
- Product Quantity:
- 200 ul
- Category:
- -
- Supplier:
- Fitzgerald
- Gene target:
- PAI1 antibody
Related genes to: PAI1 antibody
- 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: PAI1 antibody
Related articles to: PAI1 antibody
- Coronary artery disease (CAD) may progress to ischemic cardiomyopathy (ICM) and heart failure through maladaptive cardiomyocyte remodeling and myocardial fibrosis. This study aimed to identify key molecular mediators linking inflammatory and fibrotic signaling during this pathological transition. - Source: PubMed
Publication date: 2026/09/11
Chen KexinHe XingyuNing XiangmingWang YaoLi NaHu TengMa ZeyuanYang FengruiZhang YinleiMa JunShi Zheng - Cellular senescence is a complex biological process characterized by irreversible cell-cycle arrest and acquisition of the senescence-associated secretory phenotype (SASP). Beyond biochemical stress, increasing evidence indicates that mechanical cues from the extracellular microenvironment contribute to the regulation of senescence; however, the molecular mechanisms linking mechanotransduction to senescent phenotypes remain incompletely understood. SERPINE1 (plasminogen activator inhibitor-1, PAI-1) has emerged as a key mechanosensitive effector induced downstream of mechanotransduction signaling pathways. In this review, we discuss SERPINE1 as both a hallmark of cellular senescence and a functional mediator linking mechanotransduction to senescence-associated processes. Once induced, SERPINE1 contributes to cell-cycle arrest and extracellular matrix (ECM) remodeling by inhibiting plasmin-dependent proteolysis. The resulting ECM accumulation and matrix stiffening further enhance integrin-dependent mechanotransduction, promoting further SERPINE1 expression and establishing a self-reinforcing mechanobiological feedback loop. SERPINE1 also contributes to senescence-associated inflammatory signaling, which may further support the maintenance of the senescent phenotype. Together, these findings identify SERPINE1 as a mechanistic link between mechanotransduction, ECM remodeling, and cellular senescence. Pharmacological studies using PAI-1 inhibitors further support the biological importance of this pathway and suggest that SERPINE1 may represent a potential therapeutic target for senescence-associated fibrotic diseases. - Source: PubMed
Nisa Intan ChairunChantachotikul PirawanTakahata KeiAnsori Arif Nur MuhammadDeguchi Shinji - Hepatocellular carcinoma (HCC) is characterized by a high capacity for invasion and metastasis. Epithelial-mesenchymal transition (EMT) is a key mechanism that promotes tumor migration and invasion. However, the role of serine protease inhibitor 1 (SERPINE1) as a regulatory factor that may enhance tumor progression by directly modulating EMT-related gene expression in HCC has not been fully elucidated. - Source: PubMed
Publication date: 2026/08/09
Bao RunLuo ZhaoxiaGang LiaoHuang WenWu ShengXu Fangmin - Colorectal cancer (CRC) is one of the most common and lethal malignancies worldwide, and its tumor ecosystem remains highly complex and incompletely understood. Here, we analyzed 3,264 single-cell transcriptomes from primary CRC tumors obtained from nine patients in the GSE110009 dataset. We identified 15 distinct cell clusters corresponding to seven major cell types. Trajectory inference (pseudotime analysis) was performed to characterize lineage relationships and cellular developmental trajectories. Genes associated with distinct expression programs were classified into two clusters exhibiting different tumor microenvironment (TME) characteristics. Functional enrichment analysis revealed that epithelial-mesenchymal transition (EMT) plays a critical role in CRC tumorigenesis and metastasis. Moreover, we established a novel three-gene prognostic signature that effectively predicts clinical outcomes in CRC patients. Further analyses revealed that SERPINE1 promotes CRC cell invasion and metastasis by enhancing resistance to anoikis. Furthermore, SERPINE1 was found to enhance the malignant phenotype of metastatic colorectal cancer cells. Collectively, these findings reveal the immunosuppressive landscape of the CRC TME, provide new insights into CRC progression, and identify SERPINE1 as a potential prognostic biomarker and therapeutic target. - Source: PubMed
Publication date: 2026/09/19
Zhu YaruLiu DiyaRen ZhenYuan HongLai LinyingGuo Cheng - BackgroundEarly detection of sepsis-induced coagulopathy (SIC) is of great clinical significance, as its closely correlates with disease progression in patients with sepsis. In the present study, we focused on mining the major coagulation factors that participate in the development and progression of SIC, and exploring the potential regulatory networks of these core factors.MethodMeta-analysis was performed to explore the association between SIC and mortality. eQTLs significantly associate with sepsis-related 28-day mortality and pQTLs were analyzed, to mine the significant sites or genes. Mendelian randomization (MR) was then applied to evaluate the role of coagulation factors in SIC and to explore their genetic regulation via DNA sequence analysis. Moreover, QGRS Mapper combined with ThT fluorescence assays were used to detect G-quadruplexes (G4s) structures within coagulation factor genes.ResultsSepsis patients with SIC exhibited higher sequential organ failure assessment (SOFA) scores and increased 28-day mortality compared to those without SIC. MR and clinical analyses demonstrated that PAI-1 serves as a major contributor to higher sepsis incidence and 28-day mortality. Notably, the PAI-1 rs1799762 genetic polymorphism alters this biological effect. Mechanistically, G4-forming capacity negatively correlates with PAI-1 expression. In particular, the 5G/5G genotype was associated with a higher G4-forming propensity in the PAI-1 gene, which in turn weakened gene transcription and lowered PAI-1 expression relative to other genotypes.ConclusionG4s formation in the PAI-1 gene modulates circulating PAI-1 levels and may serve as a novel prognostic marker and therapeutic target for sepsis severity assessment, particularly in patients with SIC. - Source: PubMed
Publication date: 2026/09/18
Sun FangZhang SuhuaNie ZhenlinHe BangshunTang QiaoGao Tianyi