ArticleCell adhesion & migration
Ras guanyl nucleotide releasing protein 2 affects cell viability and cell-matrix adhesion in ECV304 endothelial cells.
Article in Cell adhesion & migration. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 8 citations in OpenAlex.
- Analysis of the key ligand receptor CADM1_CADM1 in the regulation of thyroid cancer based on scRNA-seq and bulk RNA-seq data.Frontiers in endocrinology · 2022Article
- The Role of RASGRP2 in Vascular Endothelial Cells-A Mini Review.International journal of molecular sciences · 2021Review
- RASGRP2 Suppresses Apoptosis via Inhibition of ROS Production in Vascular Endothelial Cells.TheScientificWorldJournal · 2019Article
- Genes and pathways associated with the occurrence of malignancy in benign lymphoepithelial lesions.Molecular medicine reports · 2018Article
- Distinct functions for Rap1 signaling in vascular morphogenesis and dysfunction.Experimental cell research · 2013Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ras guanyl nucleotide releasing proteins (RasGRPs) are guanine nucleotide exchange factors that activate Ras and Rap. We recently reported that xrasgrp2, which is a homolog of the human rasgrp2, plays a role in vasculogenesis and/or angiogenesis during early development of Xenopus embryos. However, the function of RasGRP2 in human vascular endothelium remains unknown. Therefore we aimed to analyze the function of human RasGRP2 in vascular endothelial cells. RasGRP2 overexpression did not increase Ras activation. However, it slightly increased Ras expression and increased proliferation in ECV304 cells. Furthermore, RasGRP2 overexpression increased Rap1 activation and cell-matrix adhesion in ECV304 cells. These data demonstrate that RasGRP2 increases cell viability and cell-matrix adhesion through increased Ras expression and Rap1 activation, respectively, in endothelial cells.
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Registered trials
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