Vascular endothelial cadherin (VE-cadherin) is located strictly at endothelial junctions and appears to be a major adhesive component of cell to cell contacts. Genomic clones spanning 36 kb and encompassing the mouse VE-cadherin gene have been isolated and characterized. The gene is composed of 12 exons that exhibit conventional vertebrate splicing. The first exon is entirely untranslated, and both exons 2 and 12 contain untranslated regions. A single major transcriptional start site was identified and located 75 bases upstream of the translation initiation codon in the cDNA sequence. The proximal 5'-flanking domain lacks consensus TATA and CAAT boxes at the usual positions. Exon-intron boundaries are similar to those of other cadherin genes, with some exceptions that may have a functional significance in VE-cadherin behavior. The VE-cadherin gene (locus Cdh5) maps to mouse chromosome 8, where it colocalizes with E-cadherin (locus Cdh1), P-cadherin (locus Cdh3), and M-cadherin (locus Cdh14) genes, suggesting that it might be part of a larger cluster of cadherin sequences.
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http://dx.doi.org/10.1006/geno.1996.0072 | DOI Listing |
J Biochem Mol Toxicol
January 2025
Laboratory of Translational Medicine in Microvascular Regulation, Medical Research Center, The First Affiliated Hospital of Shandong First Medical University and Shandong Provincial Qianfoshan Hospital; Shandong Provincial Key Laboratory of Medicine in Microvascular Ageing; Laboratory of Future Industry of Gene Editing in Vascular Endothelial Cells of Universities in Shandong Province, Jinan, China.
Cadmium (Cd) is a toxic heavy metal which induces vascular disorders. Previous studies suggest that Cd in the bloodstream affects vascular endothelial cells (ECs), potentially contributing to vascular-related diseases. However, the molecular mechanisms of effects of Cd on ECs remain poorly understood.
View Article and Find Full Text PDFNat Commun
January 2025
Department of Ophthalmology, Columbia University Irving Medical Center, New York, NY, USA.
Schlemm's canal endothelial cells (SECs) serve as the final barrier to aqueous humor (AQH) drainage from the eye. SECs adjust permeability to AQH outflow to modulate intraocular pressure (IOP). The broad identification of IOP-related genes implicates SECs in glaucoma.
View Article and Find Full Text PDFGene
February 2025
College of Animal Sciences, Fujian Agriculture and Forestry University, Fuzhou, Fujian 350000, China. Electronic address:
Improving egg quality and enhancing production efficiency are essential goals in poultry breeding. CDH5 encodes a cadherin involved in Ca transport in endothelial cells. The role of CDH5 in regulating duck egg quality and its mechanisms affecting Ca concentrations in duck uterine epithelial cells remains unclear.
View Article and Find Full Text PDFNat Commun
December 2024
Translational Cancer Medicine, Research Programs Unit, Biomedicum Helsinki, University of Helsinki, Helsinki, Finland.
Endothelial cells (ECs) form a tissue-specific barrier for disseminating cancer cells in distant organs. However, the molecular regulation of the ECs in the metastatic niche remains unclear. Here, we analyze using scRNA-Seq, the transcriptional reprogramming of lung ECs six hours after the arrival of melanoma cells in mouse lungs.
View Article and Find Full Text PDFSci Rep
November 2024
Key Lab of Medical Molecular Cell Biology of Shanxi Province, Institutes of Biomedical Sciences, Key Laboratory of Chemical Biology and Molecular Engineering of Ministry of Education, Shanxi University, Taiyuan, 030006, Shanxi, China.
The underlying mechanism of vascular endothelial hyperpermeability caused by decrease of endothelial junctions occurring in atherosclerosis remains elusive. Our findings identified that plasma exosomes from patients with stable coronary artery disease (Exo) contain differentially expressed miRNAs that are clustered with genes related to cell junctions, prompting us to investigate the role of Exo in regulating vascular endothelial junctions and to elucidate the underlying mechanisms. Here, we show that Exo markedly impair vascular endothelial junctions via suppressing VE-Cadherin and ZO-1 in endothelial cells in vitro and in vivo, consequently increases endothelial permeability.
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