ZNF683 293T Cell Transient Overexpression Lysate(Denatured)
- Known as:
- ZNF683 293T Cell Transient Overexpression Lysate(Denatured)
- Catalog number:
- H00257101-T01
- Product Quantity:
- 100 uL
- Category:
- -
- Supplier:
- Abno
- Gene target:
- ZNF683 293T Cell Transient Overexpression Lysate(Denatured)
Related genes to: ZNF683 293T Cell Transient Overexpression Lysate(Denatured)
- Gene:
- ZNF683 NIH gene
- Name:
- zinc finger protein 683
- Previous symbol:
- -
- Synonyms:
- MGC33414, Hobit
- Chromosome:
- 1p36.11
- Locus Type:
- gene with protein product
- Date approved:
- 2005-03-31
- Date modifiied:
- 2015-08-26
Related products to: ZNF683 293T Cell Transient Overexpression Lysate(Denatured)
Related articles to: ZNF683 293T Cell Transient Overexpression Lysate(Denatured)
- Human papillomavirus-positive oropharyngeal squamous cell carcinoma (HPV + OPSCC) generally has favorable outcomes yet remains prone to late recurrence. Durable control likely depends on persistent tumor-specific CD8+ T cells, but their persistence and function in metastasis are poorly understood. - Source: PubMed
Publication date: 2026/07/26
Ishihara HiromasaShibata HirofumiMuraoka DaisukeDemachi-Okamura AyakoOkamoto TakanariMizuta RyoFukushima YasunoriSugita YusukeOgasawara AikoNishida ReinaBeppu ShintaroTerada HoshinoNishikawa DaisukeSuzuki HidenoriMasago KatsuhiroSasaki EiichiSakakura NoriakiYamaguchi RuiHanai NobuhiroOgawa TakenoriMatsushita Hirokazu - Metabolic syndrome (MetS) has been associated with increased acute pancreatitis (AP) severity. This study aimed to identify shared differentially expressed genes (CDEGs) between MetS and AP and to prioritize mechanistically relevant targets. The shared genetic basis and causal effect of MetS on AP were first assessed using linkage disequilibrium score regression (LDSC) and two-sample Mendelian randomization (MR). Public Gene Expression Omnibus (GEO) datasets were analyzed to define shared CDEGs. A multi-step pipeline incorporating functional enrichment, protein-protein interaction (PPI) analysis, and transcription factor mapping was used to identify AP hub genes (AP-HGs). Functional relatedness and putative causal relationships were evaluated using GeneMANIA, MR, and single-cell RNA sequencing (scRNA-seq). Finally, computational drug prediction and molecular docking were performed to identify potential therapeutic agents. Key findings were further validated in a hyperlipidemia AP (HAP) model. A positive genetic correlation between MetS and AP was identified by LDSC, and MR supported a causal effect of MetS on increased AP risk. BCAT1, GPAT3, ANP32C, and ZNF683 were identified as CDEGs between MetS and AP. MAPK14 was identified as a central AP-HG. MAPK14, BCAT1, and GPAT3 were effective predictors for severe AP (SAP), with AUCs of 0.738, 0.722, and 0.744, respectively. GeneMANIA predicted a high degree of physical interaction (77.6%) among these genes. MR analysis provided supportive genetic evidence linking MAPK14 expression to inflammatory mediators including IL-1ra and TNFR-1. scRNA-seq analysis in an experimental AP model localized Mapk14 expression predominantly to macrophages, while Bcat1 marked a unique, proliferative fibroblast subpopulation that emerged transiently during inflammation and exhibited an anabolic metabolic signature. Ozagrel was prioritized as an exploratory candidate with favorable predicted binding affinities and requires further validation. In a HAP model, aggravated pancreatic injury and upregulation of BCAT1 and MAPK14 were confirmed under the high-fat background. A genetic and transcriptomic link between MetS and AP was identified. MAPK14-associated inflammation and Bcat1-positive fibroblast remodeling may contribute to AP aggravation under metabolic disturbance. These findings provide candidate biomarkers for SAP prediction and support BCAT1 and MAPK14 as potential mechanistic targets. - Source: PubMed
Zhou XiaoyingYang ChenZou TongxinBasharat ZarrinZippi MaddalenaFiorino SirioHong Wandong - Alopecia areata (AA) is an autoimmune disorder characterized by hair loss due to immune-mediated destruction of hair follicles. The polygenic nature of AA, influenced by genetic and environmental factors, complicates its pathogenesis. Advances in bioinformatics have facilitated understanding of AA's genetic basis, providing insights into key molecular pathways and regulatory mechanisms. - Source: PubMed
Publication date: 2026/06/28
AbdElneam Ahmed IbrahimAl-Dhubaibi Mohammed SalehBahaj Saleh SalemMohammed Ghada FaroukAtef Lina Mohammed - Lymphovascular space invasion (LVSI) is a critical factor linked to metastasis and poor outcomes in endometrioid endometrial carcinoma (EEC), yet its multicellular mechanisms remain unclear. Using single-cell RNA sequencing of 3 LVSI-present (LVSI+) EECs, 2 LVSI-absent (LVSI-) EECs, and 2 normal endometrial samples, we delineated the cellular ecosystems underlying LVSI. LVSI+ EECs exhibited marked epithelial reprogramming, transitioning from differentiated ciliated epithelium to hyperproliferative and metabolically remodelled phenotypes, and contained TC4, a metastatic epithelial subset characterized by hypoxia, partial epithelial-mesenchymal transition, immunosuppression, and progesterone resistance. We also identified nine key genes in malignant epithelial cells associated with LVSI prognosis. The tumour microenvironment in LVSI+ EECs shifted from an inflammatory state dominated by epithelial cells to a collaborative network involving stromal and immune cells. This network was enriched in immunosuppressive ZNF683 + SOX4 + CD8+ T cells, Cycling_T cells, SPP1 + MMP9 + Mac, WNT5A_mCAF, Tip endothelial cells, and lymphatic endothelial cells. WNT5A_mCAF and SPP1 + MMP9 + Mac synergistically remodelled the extracellular matrix, promoted lymphangiogenesis and angiogenesis, and, together with endothelial cells, suppressed T-cell activity via LGALS9-HAVCR2/CD44 inhibitory signalling, thereby establishing a niche conducive to vascular invasion. Using spatial multiplex immunofluorescence, we confirmed hypoxic tumour epithelial cells at the invasive front coexisting with an immunosuppressive microenvironment, and revealed spatial colocalization of PD-L1+ tumour cells, PD-L1+ macrophages, and PD-1+ T cells within LVSI thrombi. Our comprehensive study provides deeper insights into LVSI as an actively coordinated multicellular process, potentially improving LVSI risk prediction, supporting treatment decision-making, and informing new therapies targeting the tumour microenvironment. - Source: PubMed
Publication date: 2026/06/23
Guo WendiLiu TianxiangRen RunlingLi NaZhang WenwenSi JingwenPiao YongjunHu Yuanjing - Checkpoint inhibitor pneumonitis (CIP) is the leading cause of treatment-related deaths for immune checkpoint inhibitor (ICI) combination therapies. CIP is problematic to diagnose and differentiate, particularly from radiation pneumonitis (RP), due to the lack of mechanistic distinctions between them. - Source: PubMed
Publication date: 2026/06/09
Zhou XiaoxiangJiang ZimingRen YanhongZhou YunzhiDeng LeiLiu ZhentingSun SijinZhang JieliLiu WenyangYang YinRen WentingWang YanfengLi HongxiaLi YiqunMa FeiBi NanWang LuhuaGao YiboHe Jie