CDH5 antibody
- Known as:
- CDH5 (anti-)
- Catalog number:
- orb42259
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- CDH5 antibody
Related genes to: CDH5 antibody
- 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: CDH5 antibody
Related articles to: CDH5 antibody
- Triple-negative breast cancer (TNBC) is an aggressive subtype associated with high metastatic potential and poor outcomes, with lung metastasis representing one of the most frequent and life-threatening events. However, the mechanism how cellular plasticity and reprogramming that enable TNBC cells to colonize in the lung remain incompletely understood. Here, we integrated single-cell RNA sequencing and spatial transcriptomics on paired MMTV-PyMT primary mammary tumors and lung metastatic tumors, complemented by functional assays in 4T1 mouse models, to delineate the cellular heterogeneity and molecular mechanisms driving TNBC lung metastasis. We identified three metastasis-associated subtypes-C12-Cd, Cdh5-like, and Wfdc12-each enriched in metastatic lesions and exhibiting distinct biological programs. The C12-Cd subcluster was characterized by the upregulation of Exoc4, a vesicle-trafficking regulator associated with a poor prognosis in patients with TNBC. The Cdh5-like cluster displayed a hypoxia-driven vascular phenotype, in which Hif-2α-mediated Cd36 expression promoted vasculogenic mimicry and metastatic colonization. The Wfdc12 cluster secreted Cxcr2 ligands (Cxcl1/2) and Cxcr2 blockade significantly reduced lung metastasis in vivo, underscoring therapeutic potential. Notably, cross-subtypes of lung metastatic TNBC analysis revealed Sftpc upregulation, reflecting organ-adaptive transcriptional reprogramming that may facilitate tumor cell survival in the pulmonary niche. Collectively, our findings provide a comprehensive cellular and molecular atlas of TNBC lung metastasis. We establish Exoc4, the Hif-2α-Cd36 vasculogenic mimicry axis, Cxcrl1/2-Cxcr2 signaling, and Sftpc as critical mediators of metastatic adaptation. These results not only bridge key knowledge gaps in metastatic heterogeneity and organ-specific adaptation but also highlight novel prognostic markers and therapeutic vulnerabilities with translational potential for treating TNBC lung metastasis. - Source: PubMed
Publication date: 2026/07/07
Lee Hsiao-ChenKuo Chia-YuChen Fang-MingHou Ming-FengTsai Hung-PeiWu Yu-YuanChuang Kai-ChienWu Ling-YuPan Sheng-FengTsai Ying-MingHsu Ya-Ling - Lagopsis supina is a traditional Chinese medicinal herb used for activating blood circulation and nourishing the blood. This study aims to investigate the pro-angiogenic constituents of L. supina and their mechanisms of their action. 30 compounds derived from the active fraction LS-D (L. supina 60% ethanol-water extract) were screened, of which 15 showed angiogenesis-promoting activity, were screened in a PTK787-induced vascular injury zebrafish model. The active constituents were primarily phenolic acids and phenylpropanoids, among which compounds LS21 (vanillic acid) and LS22 (syringic acid) exhibited the most potent pro-angiogenic effects. These constituents (LS21 and LS22) were selected for further investigation of mechanisms of promoting angiogenesis. Transcriptomic analysis followed by Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment revealed differentially expressed genes and predicted involved pathways. Molecular docking simulated interactions between compounds and key pathway proteins, and RT-qPCR validated gene expression patterns. Mechanistic studies integrating transcriptomics, molecular docking, and RT-qPCR revealed that both LS21 and LS22 downregulated immune-related cell adhesion molecules, while upregulating cdh5 and pecam1a. Additionally, LS21 specifically downregulated the signaling molecules smad2 and smad3a, and upregulated the transcriptional corepressors skila and ncor1. In contrast, LS22 downregulated extracellular matrix-related adhesion molecules and itga2b, while upregulating thbs1a and integrin itgb3b. In conclusion, the L. supina constituents LS21 and LS22 that are primarily phenolic acids and phenylpropanoids, exert their angiogenesis-promoting effects mainly via modulating cell adhesion and suppressing TGF-β signaling pathway. - Source: PubMed
Publication date: 2026/07/06
Yu JiahaoWang XiaoyiJia LiyanFu LuluHe JunweiZhang ShanshanHe QiuxiaLiu KechunLi XiaobinLi Na - 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 (NPR-C) 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