ArticleOncogene2003
The protein-tyrosine phosphatase DEP-1 modulates growth factor-stimulated cell migration and cell-matrix adhesion.
Article in Oncogene, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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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.
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Who cites it
26 citing papers in PubMed, 55 citations in OpenAlex.
- CD148 agonistic antibody alleviates renal injury induced by chronic angiotensin II infusion in mice.BMC nephrology · 2025Article
- Promoting the activity of a receptor tyrosine phosphatase with a novel pH-responsive transmembrane agonist inhibits cancer-associated phenotypes.Protein science : a publication of the Protein Society · 2023Article
- The effects of CD148 Q276P/R326Q polymorphisms in A431D epidermoid cancer cell proliferation and epidermal growth factor receptor signaling.Cancer reports (Hoboken, N.J.) · 2022Article
- Disrupting PTPRJ transmembrane-mediated oligomerization counteracts oncogenic receptor tyrosine kinase FLT3 ITD.Frontiers in oncology · 2022Article
- Agonistic anti-CD148 monoclonal antibody attenuates diabetic nephropathy in mice.American journal of physiology. Renal physiology · 2020Article
- Growth Factor Deregulation and Emerging Role of Phosphatases in Diabetic Peripheral Artery Disease.Frontiers in cardiovascular medicine · 2020Review
- R3 receptor tyrosine phosphatases: conserved regulators of receptor tyrosine kinase signaling and tubular organ development.Seminars in cell & developmental biology · 2015Review
- The phosphatase CD148 promotes airway hyperresponsiveness through SRC family kinases.The Journal of clinical investigation · 2013Article
- Knockout of Density-Enhanced Phosphatase-1 impairs cerebrovascular reserve capacity in an arteriogenesis model in mice.BioMed research international · 2013Article
- Association of the protein-tyrosine phosphatase DEP-1 with its substrate FLT3 visualized by in situ proximity ligation assay.PloS one · 2013Article
- Expression and function of the protein tyrosine phosphatase receptor J (PTPRJ) in normal mammary epithelial cells and breast tumors.PloS one · 2012Article
- Loss of the protein-tyrosine phosphatase DEP-1/PTPRJ drives meningioma cell motility.Brain pathology (Zurich, Switzerland) · 2011Article
- Article
- Protein-tyrosine phosphatase DEP-1 controls receptor tyrosine kinase FLT3 signaling.The Journal of biological chemistry · 2011Article
- 12/15-lipoxygenase-derived lipid peroxides control receptor tyrosine kinase signaling through oxidation of protein tyrosine phosphatases.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
- The Eyes Absent phosphatase-transactivator proteins promote proliferation, transformation, migration, and invasion of tumor cells.Oncogene · 2010Article
- An unbiased screen identifies DEP-1 tumor suppressor as a phosphatase controlling EGFR endocytosis.Current biology : CB · 2009Article
- Physiological signaling specificity by protein tyrosine phosphatases.Physiology (Bethesda, Md.) · 2009Review
- Tumor suppressor density-enhanced phosphatase-1 (DEP-1) inhibits the RAS pathway by direct dephosphorylation of ERK1/2 kinases.The Journal of biological chemistry · 2009Article
- The structure of the 5'-end of the protein-tyrosine phosphatase PTPRJ mRNA reveals a novel mechanism for translation attenuation.Nucleic acids research · 2008Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Density-enhanced protein-tyrosine phosphatase-1 (DEP-1 also CD148) is a transmembrane molecule with a single intracellular PTP domain. It has recently been proposed to function as a tumor suppressor. We have previously shown that DEP-1 dephosphorylates the activated platelet-derived growth factor (PDGF) beta-receptor in a site-selective manner (Kovalenko et al. (2000). J. Biol. Chem. 275, 16219-16226). We analysed cell lines with inducible DEP-1 expression for cellular functions of DEP-1. Several aspects of PDGFbeta-receptor signaling were negatively affected by DEP-1 expression. These include PDGF-stimulated activation of inositol trisphosphate formation, Erk1/2, p21Ras, and Src. Activation of receptor-associated phosphoinositide-3 kinase activity and of Akt/PKB were weakly attenuated at early time points of stimulation. Inhibition of PDGF-stimulated signaling depended on DEP-1 catalytic activity. Importantly, DEP-1 inhibited PDGF-stimulated cell migration. The catalytically inactive DEP-1 C1239S variant enhanced cell migration and PDGF-stimulated Erk1/2 activation, suggesting a dominant negative interference with endogenous DEP-1. In contrast to cell migration, cell-substrate adhesion was promoted by active DEP-1 and delayed or suppressed by DEP-1 C1239S, correlating with positive effects of DEP-1 on adhesion-stimulated Src kinase. We propose that negative regulation of growth-factor stimulated cell migration and promotion of cell-matrix adhesion may be related to the function of DEP-1 as tumor suppressor.
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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.