Mouse Cadherin 5 ELISA ,CDH5
- Known as:
- Mouse Cadherin 5 Enzyme-linked immunosorbent assay test ,CDH5
- Catalog number:
- E03C0500
- Product Quantity:
- 96 Tests/kit
- Category:
- -
- Supplier:
- BGene
- Gene target:
- Mouse Cadherin 5 ELISA CDH5
Related genes to: Mouse Cadherin 5 ELISA ,CDH5
- Gene:
- CDH5 NIH gene
- Name:
- cadherin 5
- Previous symbol:
- -
- Synonyms:
- 7B4, CD144
- Chromosome:
- 16q21
- Locus Type:
- gene with protein product
- Date approved:
- 1992-11-20
- Date modifiied:
- 2016-10-05
Related products to: Mouse Cadherin 5 ELISA ,CDH5
Related articles to: Mouse Cadherin 5 ELISA ,CDH5
- Given the high relevance of human cardiac valve disease, recent research aims to differentiate human induced pluripotent stem cells (hiPSCs) into valve endothelial-like cells (VELCs) and, through endothelial-to-mesenchymal transition (EndMT), into valve interstitial-like cells (VILCs). - Source: PubMed
Publication date: 2026/07/02
Farzaneh ZBrückner AFleischmann B KRieck S - Tumor-associated endothelial cells (TAECs) are integral components of the clear cell renal cell carcinoma (ccRCC) microenvironment, but their gene expression-based prognostic value and functional relevance remain to be defined. - Source: PubMed
Publication date: 2026/07/02
Liu QingCao WenxingHao Zhouhua - Obesity-induced insulin resistance contributes to metabolic dysfunction and type 2 diabetes, yet the endothelial mechanisms involved remain incompletely understood. Here, we identify endothelial natriuretic peptide receptor C (NPRC) as a key regulator of insulin transport and insulin sensitivity. NPR-C expression was increased in endothelial cells from adipose tissue and skeletal muscle of obese mice. Endothelial-specific deletion of NPR-C improved insulin sensitivity, whereas endothelial NPR-C overexpression aggravated insulin resistance, as demonstrated by glucose tolerance, insulin tolerance, and hyperinsulinemic-euglycemic clamp. Mechanistically, NPR-C impaired insulin uptake and transendothelial transport by reducing insulin receptor (IR) membrane localization and altering intracellular trafficking. NPR-C directly interacted with Caveolin-1 and promoted Tyr14 phosphorylation-dependent K48-linked ubiquitination and proteasomal degradation of Caveolin-1, disrupting caveolae function and impairing IR trafficking. Importantly, Cdh5 promoter-driven adeno-associated virus-mediated NPR-C knockdown improved insulin sensitivity in mice with established obesity. Together, these findings identify endothelial NPR-C as a regulator of Caveolin-1 stability and IR trafficking and suggest NPR-C as a potential therapeutic target for obesity-associated insulin resistance. - Source: PubMed
Publication date: 2026/06/30
Xu Zi-QiYu Xin-YiWei Jin-QiuDeng Qian-WanZhai Wen-HuiRong Wu-WeiLi Meng-YaoZhang Qi-RongGao Ping-JinLi Xiao-DongWang Ji-Guang - Oral squamous cell carcinoma (OSCC) is characterized by high aggressiveness. This study aims to elucidate the role of NDRG1 in the evolutionary heterogeneity and spatial microenvironmental remodelling of OSCC. By integrating bulk transcriptomics, single-cell RNA sequencing (scRNA-seq), and spatial transcriptomics (ST), complemented by in vivo and in vitro functional assays, we systematically explored the regulatory logic of the MSTRG.47889/miR-1299/NDRG1 axis. The MSTRG.47889/miR-1299/NDRG1 ceRNA regulatory axis was identified and validated, demonstrating its significant role in promoting OSCC proliferation and invasion while impairing cellular adhesion. Single-cell analysis revealed a significant expansion of the NDRG1-high subpopulation in tumour tissues, which drives cellular evolution along a pseudotime trajectory toward a partial epithelial-mesenchymal transition (p-EMT) and a high glycolytic state. Spatial transcriptomics analysis revealed that NDRG1 is highly expressed within 'hypoxia-metabolic' niches. Our integrative analysis suggests that these regions may coordinate with endothelial cells, highlighting a potential role for the ANGPTL4-CDH5 signalling axis in promoting a proangiogenic microenvironment. These findings provide preliminary insights into how NDRG1 serves as a pivotal regulator driving p-EMT and coordinating niche remodelling. NDRG1 serves as a pivotal regulator driving p-EMT and proangiogenic niche remodelling, representing a potential novel target for the diagnosis and treatment of OSCC. - Source: PubMed
Publication date: 2026/06/27
Feng LeiOu YiTian LinqingJiang WenjieZhang MinSheng Xun - Breast cancer (BC) and non-small cell lung carcinoma (NSCLC) are two of the most prevalent and lethal malignancies, with shared molecular alterations that could serve as biomarkers for diagnosis and therapy. We employed integrated bioinformatics approaches to identify common hub genes in both cancers by analyzing eight GEO transcriptomic datasets. The protein-protein interaction network revealed ten hub genes: five upregulated (TOP2A, CCNB1, CCNB2, MELK, and UBE2C) and five downregulated (CDH5, MMRN2, RAMP2, CCM2L, and CD36), which were validated through transcriptomic analyses. These genes were associated with key process such as cell-cycle regulation, DNA replication, angiogenesis, and endothelial integrity. Among the hub genes analyzed, significant survival associations were observed for selected genes in a cancer-type-specific manner, particularly for several upregulated hub genes in LUAD, whereas most hub genes showed no statistically significant association with overall survival. Molecular docking results demonstrated favorable interactions between WGX-50 and these targets, with the top vina scores indicating a strong binding affinity. Subsequent molecular dynamics simulations of WGX-50 with CD36 and MELK confirmed stable interactions, involving hydrogen bonds, hydrophobic interactions, and water bridges. These findings highlight the therapeutic potential of WGX-50 as a multitarget anticancer agent capable of modulating multiple signaling cascades. This Insilico study provides valuable insights into the development of targeted therapies for BC, NSCLC, and presents WGX-50 as a promising anticancer candidate. - Source: PubMed
Publication date: 2026/06/25
Farooq AdilRizwan MuhammadYousaf NumanImran MuhammadJin MengyuanYang YiliangWei Dongqing