ArticleBlood2011
Density enhanced phosphatase-1 down-regulates urokinase receptor surface expression in confluent endothelial cells.
Article in Blood, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
20 citing papers in PubMed, 36 citations in OpenAlex.
- MiR-362-3p inhibits the proliferation, migration and EMT of gastric cancer cells by regulating the DEP-1/ERK signaling pathway.Scientific reports · 2026Article
- Endothelial-specific Enhancer as a Cis Element ofCurrent pharmaceutical design · 2024Review
- Endothelial Senescence and Its Impact on Angiogenesis in Alzheimer's Disease.International journal of molecular sciences · 2023Review
- Article
- uPAR-expressing melanoma exosomes promote angiogenesis by VE-Cadherin, EGFR and uPAR overexpression and rise of ERK1,2 signaling in endothelial cells.Cellular and molecular life sciences : CMLS · 2021Article
- CRISPR/Cas9 uPAR Gene Knockout Results in Tumor Growth Inhibition, EGFR Downregulation and Induction of Stemness Markers in Melanoma and Colon Carcinoma Cell Lines.Frontiers in oncology · 2021Article
- IGF-1C domain-modified hydrogel enhanced the efficacy of stem cells in the treatment of AMI.Stem cell research & therapy · 2020Article
- Article
- Targeting Receptor-Type Protein Tyrosine Phosphatases with Biotherapeutics: Is Outside-in Better than Inside-Out?Molecules (Basel, Switzerland) · 2018Review
- A novel splice variant of the protein tyrosine phosphatase PTPRJ that encodes for a soluble protein involved in angiogenesis.Oncotarget · 2017Article
- Article
- Lipid rafts: integrated platforms for vascular organization offering therapeutic opportunities.Cellular and molecular life sciences : CMLS · 2015Review
- Differential uPAR recruitment in caveolar-lipid rafts by GM1 and GM3 gangliosides regulates endothelial progenitor cells angiogenesis.Journal of cellular and molecular medicine · 2015Article
- Immunocytochemical and biochemical detection of the urokinase-type plasminogen activator receptor (uPAR) in the rat tooth germ and in lipid rafts of PMA-stimulated dental epithelial cells.Histochemistry and cell biology · 2013Article
- Domain 2 of uPAR regulates single-chain urokinase-mediated angiogenesis through β1-integrin and VEGFR2.American journal of physiology. Heart and circulatory physiology · 2013Article
- A computational model predicting disruption of blood vessel development.PLoS computational biology · 2013Article
- VEGF-induced endothelial cell migration requires urokinase receptor (uPAR)-dependent integrin redistribution.Cardiovascular research · 2012Article
- Angiogenesis in cancer: Anti-VEGF escape mechanisms.Translational lung cancer research · 2012Review
- Characterization of the endothelial cell cytoskeleton following HLA class I ligation.PloS one · 2012Article
- VEGF-initiated angiogenesis and the uPA/uPAR system.Cell adhesion & migrationReview
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
VEGF(165), the major angiogenic growth factor, is known to activate various steps in proangiogenic endothelial cell behavior, such as endothelial cell migration and invasion, or endothelial cell survival. Thereby, the urokinase-type plasminogen activator (uPA) system has been shown to play an essential role not only by its proteolytic capacities, but also by induction of intracellular signal transduction. Therefore, expression of its cell surface receptor uPAR is thought to be an essential regulatory mechanism in angiogenesis. We found that uPAR expression on the surface of confluent endothelial cells was down-regulated compared with subconfluent proliferating endothelial cells. Regulation of uPAR expression was most probably affected by extracellular signal-regulated kinase 1/2 (ERK1/2) activation, a downstream signaling event of the VEGF/VEGF-receptor system. Consistently, the receptor-like protein tyrosine phosphatase DEP-1 (density enhanced phosphatase-1/CD148), which is abundantly expressed in confluent endothelial cells, inhibited the VEGF-dependent activation of ERK1/2, leading to down-regulation of uPAR expression. Overexpression of active ERK1 rescued the DEP-1 effect on uPAR. That DEP-1 plays a biologic role in angiogenic endothelial cell behavior was demonstrated in endothelial cell migration, proliferation, and capillary-like tube formation assays in vitro.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.