Ask about this productRelated genes to: SERPINE1 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: SERPINE1 antibody
Related articles to: SERPINE1 antibody
- AD is a neurodegenerative disorder marked by progressive cognitive decline, particularly memory impairment, largely driven by cholinergic dysfunction. This study aimed to investigate the pharmacological basis and modes of action of the identified TT-TeMac™ compounds againsts cholinergic dysfunction associated with memory loss. TT-TeMac™ compounds targets which were identified by LC-MS were extracted from SwissTarget Prediction and PharmMapper, while cholinergic dysfunction-related targets were obtained from DisGeNET and GeneCards. Fifteen common targets were identified, with nine key targets highlighted by STRING, Cytoscape, and Venny analyses and confirmed by molecular docking using MOE. The validation used a rat model with scopolamine-induced cholinergic dysfunction (1 mg/kg bw/day, ip) for 7 days. Subsequently, behavioral (NOR and MWM), biochemical (AchE and BuhE) and histological (H&E and CV) analyses were performed. Seven compounds were identified in TT-TeMac™ (terminolic acid, sericic acid, arjunolic acid, gallic acid, ellagic acid, 3-O-methyl ellagic acid and 3,3'-di-O-methyl ellagic acid). Network pharmacological analysis showed that TT-TeMac™ acted on 15 common targets of which ACHE, IL6, TNF, SNCA, AKT1, SERPINE1, STAT3, ACE, and ALB were the pivotal genes. Also, docking studies confirmed the involvement of the target within the network with meaningful binding energies. Furthermore, TT-TeMac™ prevented cholinergic dysfunction associated with memory loss in rats by significantly reducing cholinesterase activity and protecting against morphological alterations and neuronal loss in the hippocampus. Our study shows that the ingredient TT-TeMac™ has a multi-targeted mode of action on protein targets involved in cholinergic dysfunction and counteracts this dysfunction in scopolamine-treated rats. - Source: PubMed
Publication date: 2026/08/10
Ambamba Bruno Dupon AkambaJonathan Messanga Me Ngo'oMarc Akono Fama YvesSandrine Nyabissick MondjiepReine Njayou Mbouangouore IngridEmmanuel NgarchindiLaurent Nkodo AbegaBlonde Njanjo Ejanmoua Merveille LaAlexandra Ebogo Enyegue FrançoiseElla Fils ArmandMandob Damaris EnyegueNgondi Judith Laure - Coronary artery disease (CAD) is a complex disorder influenced by endothelial dysfunction, vascular inflammation, and thrombosis. This study evaluated selected genetic variants in endothelin signaling (EDN1, PHACTR1), nitric oxide metabolism (NOS3), and fibrinolysis (SERPINE1/PAI-1) in relation to CAD susceptibility, major clinical sub-phenotypes, and disease severity in a Turkish study population. A total of 1256 individuals who underwent coronary angiography were enrolled, including 748 CAD patients and 508 non-CAD controls. Genotyping of EDN1 rs3087459, PHACTR1 rs9349379, NOS3 rs1799983, and PAI-1 4G/5G variants were performed using quantitative real-time PCR. Logistic regression, haplotype, and gene-gene interaction analyses were conducted under multiple inheritance models. The EDN1 CC genotype was significantly associated with CAD (OR = 5.759, 95% CI: 1.319-25.149, p = 0.020), severe CAD (p = 0.012), and C allele with myocardial infarction (OR = 1.640, 95% CI: 1.091-2.465, p = 0.017) in males. Moreover, the PHACTR1 GG genotype was associated with premature CAD (OR = 1.721, 95%CI: 1.076-2.753, p = 0.024), and greater angiographic severity (p < 0.05). The NOS3 T allele carrier males had an increased risk for diabetes (OR = 1.449, 95%CI:1.057-1.985 p = 0.021), and CAD complexed with diabetes (CAD-DM) (OR = 1.619, 95%CI:1.004-2.610, p = 0.048). Notably, the interaction between NOS3 and PHACTR1 variants was consistently associated with CAD, severe CAD, premature CAD, and CAD-DM, and was further supported by higher stenosis severity indices and elevated troponin levels (p < 0.05). These findings demonstrate that variation within endothelial pathways extends beyond CAD susceptibility to shape angiographic complexity and clinical severity. Notably, a synergistic interaction between PHACTR1 and NOS3 modulates CAD related phenotypes, emphasizing that coordinated pathway disturbances contribute to CAD heterogeneity more than isolated variants. - Source: PubMed
Publication date: 2026/08/22
Ozuynuk-Ertugrul Aybike SenaEkici BerkayKocak AjarCoban Neslihan - Resistance to immunotherapy in colorectal cancer (CRC) is closely linked to an immunosuppressive tumour microenvironment (TME), in which cancer-associated fibroblasts (CAFs) are key regulators. Cellular senescence and the senescence-associated secretory phenotype (SASP) are increasingly recognised as drivers of CAF activity, yet their systematic prognostic and immunomodulatory value in CRC remains poorly defined METHODS: Using transcriptomic and clinical data from the TCGA-COADREAD cohort, we screened differentially expressed cellular senescence-related genes (DE-CSRGs) and constructed a prognostic signature, externally validated in independent GEO cohorts (GSE39582). Multi-omics analyses-functional enrichment, immune-infiltration estimation, single-cell and spatial transcriptomics, and ligand-receptor inference-were integrated to characterise the associated biology, and findings were validated at the protein level by multiplex immunofluorescence and immunohistochemistry in an independent pMMR CRC cohort. - Source: PubMed
Publication date: 2026/08/20
Chen YingyingZhang YingLv Chi - Target-directed microRNA degradation (TDMD) is an emerging post-transcriptional mechanism that controls miRNA turnover, yet its role in human cancers remains largely unexplored. Here, we combine CRISPRi-mediated ZSWIM8 depletion, miRNA-seq, and AGO2-eCLIP to define the TDMD landscape across breast cancer subtypes. We identify 19 high-confidence TDMD substrates, including miR-29b-3p and miR-33a/b-5p, and show that TDMD shapes miRNA target occupancy and target repression. Integration with single-cell transcriptomics reveals that TDMD of miR-29b-3p triggered by NREP transcript is associated with transcriptional plasticity along the epithelial-mesenchymal axis and marks a stem-like subpopulation of malignat cells with tumor-initiating potential in triple-negative breast cancer. Unexpectedly, we also uncover a non-canonical TDMD mechanism, independent of ubiquitin ligase ZSWIM8 and the proteasome, which includes SERPINE1-triggered miR-30c-5p degradation, conferring paclitaxel resistance and enhancing sphere-forming potential. These findings establish target-directed microRNA degradation as a functional layer of miRNA regulation in cancer, linking miRNA decay to cellular state transitions and therapeutic response. Our results broaden the mechanistic spectrum of TDMD and provide a framework to investigate how regulated miRNA decay contributes to aggressive breast cancer phenotypes. - Source: PubMed
Publication date: 2026/08/17
Rubolino CarmelaD'Onghia ManfrediTordonato ChiaraSabò AriannaD'Agnelli AlessandroBisi SaraGiambruno RobertoGiuliani BiancaMarzi Matteo JacopoNicassio Francesco - Recurrent respiratory papillomatosis (RRP) is an HPV-associated airway disease with incompletely defined inflammatory and tissue-remodeling programs. - Source: PubMed
Publication date: 2026/08/11
Ma YunWang XiaojieZhang YongjuLi QingliangDou Fenfen