ArticleThe Biochemical journal1995
Increase in receptor-like protein tyrosine phosphatase activity and expression level on density-dependent growth arrest of endothelial cells.
Article in The Biochemical journal, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 60 citations in OpenAlex.
- G0 or no-G0: phosphatase control of quiescence and cell cycle entry.Biochemical Society transactions · 2026Review
- R-PTP-κ Inhibits Contact-Dependent Cell Growth by Suppressing E2F Activity.Biomedicines · 2022Article
- 12/15-Lipoxygenase-derived lipid metabolites induce retinal endothelial cell barrier dysfunction: contribution of NADPH oxidase.PloS one · 2013Article
- Receptor protein tyrosine phosphatase micro regulates the paracellular pathway in human lung microvascular endothelia.The American journal of pathology · 2005Article
- Vascular endothelial-cadherin tyrosine phosphorylation in angiogenic and quiescent adult tissues.Circulation research · 2005Article
- Function analysis of estrogenically regulated protein tyrosine phosphatase gamma (PTPgamma) in human breast cancer cell line MCF-7.Oncogene · 2004Article
- Natural antibody-induced intracellular signalling and growth control in C3H 10T1/2 fibroblast variants.Immunology · 2000Article
- Functional interaction of vascular endothelial-protein-tyrosine phosphatase with the angiopoietin receptor Tie-2.Oncogene · 1999Article
- The supporting-cell antigen: a receptor-like protein tyrosine phosphatase expressed in the sensory epithelia of the avian inner ear.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1999Article
- Thrombospondin-1 induces tyrosine phosphorylation of adherens junction proteins and regulates an endothelial paracellular pathway.Molecular biology of the cell · 1999Article
- Confluence of vascular endothelial cells induces cell cycle exit by inhibiting p42/p44 mitogen-activated protein kinase activity.Molecular and cellular biology · 1999Article
- E-Cadherin-dependent growth suppression is mediated by the cyclin-dependent kinase inhibitor p27(KIP1).The Journal of cell biology · 1998Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Protein tyrosine phosphatase (PTPase) activity was examined in two cell lines: human umbilical vein endothelial (HUVE) cells, which display contact inhibition of cell growth, and A427 human adenocarcinoma cells, which have lost this ability. HUVE cells harvested at high density displayed a 10-fold increase in membrane-associated PTPase activity. A427 cells exhibited no such phenomenon. Moreover, modification of HUVE cell growth rate by a stimulating agent such as basic fibroblast growth factor or by blocking compounds such as thymidine or suramin resulted in no change in PTPase activity, suggesting that the observed increase in membrane-associated activity at confluency was specific for cell-cell-contact-directed growth arrest. The expression of various PTPase mRNAs was examined in HUVE and A427 cells. Of the receptor-like PTPases tested, two were exclusively expressed in HUVE cells (PTP gamma and HPTP beta). Only HPTP beta, which is structurally similar in its extracellular region to cell-adhesion receptors of the immunoglobulin superfamily, displayed a pattern of expression related to the increase in PTPase activity. Competitive PCR was used to quantify its expression during cell culture. A 12-fold increase in HPTP beta mRNA expression was detected and it parallelled the time course of PTPase activity. This observation strongly implicates receptor-like PTPases in density-dependent growth arrest.
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