Genomes and Genes
Gene Symbol: Ptprj
Description: protein tyrosine phosphatase, receptor type, J
Alias: DEP-1, receptor-type tyrosine-protein phosphatase eta, density enhanced phosphatase-1
- Takahashi T, Takahashi K, St John P, Fleming P, Tomemori T, Watanabe T, et al. A mutant receptor tyrosine phosphatase, CD148, causes defects in vascular development. Mol Cell Biol. 2003;23:1817-31 pubmed..These findings implicate a member of the receptor tyrosine phosphatase family, CD148, in developmental vascular organization and provide evidence that it regulates endothelial proliferation and endothelium-pericyte interactions. ..
- Citri A, Yarden Y. EGF-ERBB signalling: towards the systems level. Nat Rev Mol Cell Biol. 2006;7:505-16 pubmed..Because network fragility is an inevitable trade-off of robustness, systems-level understanding is expected to generate therapeutic opportunities to intercept aberrant network activation. ..
- Balavenkatraman K, Jandt E, Friedrich K, Kautenburger T, Pool Zobel B, Ostman A, et al. DEP-1 protein tyrosine phosphatase inhibits proliferation and migration of colon carcinoma cells and is upregulated by protective nutrients. Oncogene. 2006;25:6319-24 pubmed..Upregulation of DEP-1 expression, and in turn inhibition of cell growth and migration may present a previously unrecognized mechanism of chemoprevention by nutrients. ..
- Dave R, Hume D, Elsegood C, Kellie S. CD148/DEP-1 association with areas of cytoskeletal organisation in macrophages. Exp Cell Res. 2009;315:1734-44 pubmed publisher..There were no detectable effects on the CSF-1 receptor-akt signalling pathway. These results are consistent with the hypothesis that CD148 is a regulator of macrophage activity. ..
- Chabot C, Spring K, Gratton J, Elchebly M, Royal I. New role for the protein tyrosine phosphatase DEP-1 in Akt activation and endothelial cell survival. Mol Cell Biol. 2009;29:241-53 pubmed publisher..Overall, our results reveal that despite its negative role on global VEGFR2 phosphorylation, DEP-1 is a positive regulator of VEGF-mediated Src and Akt activation and endothelial cell survival. ..
- Chin C, Sachs J, Engelman D. Transmembrane homodimerization of receptor-like protein tyrosine phosphatases. FEBS Lett. 2005;579:3855-8 pubmed..Through a mutational study of the DEP1 TMD, we demonstrate that these interactions are specific. Taken together, our results define a subset of the RPTP family in which TM homodimerization may act as a mediator of protein function. ..
- Borges L, Seifert R, Grant F, Hart C, Disteche C, Edelhoff S, et al. Cloning and characterization of rat density-enhanced phosphatase-1, a protein tyrosine phosphatase expressed by vascular cells. Circ Res. 1996;79:570-80 pubmed..The deduced structure and the regulation of expression of rDEP-1 suggest that it may play a role in adhesion and/or signaling events involving cell-cell and cell-matrix contact. ..
- Sallee J, Burridge K. Density-enhanced phosphatase 1 regulates phosphorylation of tight junction proteins and enhances barrier function of epithelial cells. J Biol Chem. 2009;284:14997-5006 pubmed publisher..These data suggest that DEP-1 can modify the phosphorylation state of tight junction proteins and play a role in regulating permeability. ..
- Sacco F, Tinti M, Palma A, Ferrari E, Nardozza A, Hooft van Huijsduijnen R, et al. Tumor suppressor density-enhanced phosphatase-1 (DEP-1) inhibits the RAS pathway by direct dephosphorylation of ERK1/2 kinases. J Biol Chem. 2009;284:22048-58 pubmed publisher..Overall this study provides novel insights into the anti-proliferative role of this phosphatase and proposes a new mechanism that may also be relevant for the regulation of density-dependent growth inhibition. ..
- Jandt E, Denner K, Kovalenko M, Ostman A, Bohmer F. The protein-tyrosine phosphatase DEP-1 modulates growth factor-stimulated cell migration and cell-matrix adhesion. Oncogene. 2003;22:4175-85 pubmed..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. ..
- Grazia Lampugnani M, Zanetti A, Corada M, Takahashi T, Balconi G, Breviario F, et al. Contact inhibition of VEGF-induced proliferation requires vascular endothelial cadherin, beta-catenin, and the phosphatase DEP-1/CD148. J Cell Biol. 2003;161:793-804 pubmed..In sparse cells or in VE-cadherin-null cells, this phenomenon cannot occur and the receptor is fully activated by the growth factor. ..
- Persson C, Engstrom U, Mowbray S, Ostman A. Primary sequence determinants responsible for site-selective dephosphorylation of the PDGF beta-receptor by the receptor-like protein tyrosine phosphatase DEP-1. FEBS Lett. 2002;517:27-31 pubmed..DEP-1 site-selective dephosphorylation of PDGF beta-receptor is thus determined by the primary sequence surrounding phosphorylation sites and involves interactions with residues spanning at least between positions -1 and +3. ..
- Tarcic G, Boguslavsky S, Wakim J, Kiuchi T, Liu A, Reinitz F, et al. An unbiased screen identifies DEP-1 tumor suppressor as a phosphatase controlling EGFR endocytosis. Curr Biol. 2009;19:1788-98 pubmed publisher..We report the identification of PTPRK and PTPRJ (density-enhanced phosphatase-1 [DEP-1]) as EGFR-targeting phosphatases...
- Omerovic J, Clague M, Prior I. Phosphatome profiling reveals PTPN2, PTPRJ and PTEN as potent negative regulators of PKB/Akt activation in Ras-mutated cancer cells. Biochem J. 2010;426:65-72 pubmed publisher..with similar potencies including PTPN2 (T-cell protein tyrosine phosphatase; also known as TC-PTP) and PTPRJ (protein tyrosine phosphatase receptor type J; also known as DEP-1/CD148)...
- Gobert R, Joubert L, Curchod M, Salvat C, Foucault I, Jorand Lebrun C, et al. Convergent functional genomics of oligodendrocyte differentiation identifies multiple autoinhibitory signaling circuits. Mol Cell Biol. 2009;29:1538-53 pubmed publisher..Oligodendrocytic differentiation feedback loops may therefore yield pharmacological targets to treat disease related to dysfunctional myelin deposition. ..
- Massa A, Barbieri F, Aiello C, Arena S, Pattarozzi A, Pirani P, et al. The expression of the phosphotyrosine phosphatase DEP-1/PTPeta dictates the responsivity of glioma cells to somatostatin inhibition of cell proliferation. J Biol Chem. 2004;279:29004-12 pubmed..In conclusion we propose that the expression and activation of DEP-1/PTPeta is required for somatostatin inhibition of glioma proliferation. ..
- Arena S, Pattarozzi A, Massa A, Esteve J, Iuliano R, Fusco A, et al. An intracellular multi-effector complex mediates somatostatin receptor 1 activation of phospho-tyrosine phosphatase eta. Mol Endocrinol. 2007;21:229-46 pubmed..In particular the sequential activation of JAK2, SHP-2, and Src conveys the molecular signaling from SSTR1 to the activation of this phosphatase that is responsible for the final biological effects of SST. ..
- Iervolino A, Iuliano R, Trapasso F, Viglietto G, Melillo R, Carlomagno F, et al. The receptor-type protein tyrosine phosphatase J antagonizes the biochemical and biological effects of RET-derived oncoproteins. Cancer Res. 2006;66:6280-7 pubmed..We showed previously that the expression of the receptor-type protein tyrosine phosphatase J (PTPRJ) is suppressed in neoplastically transformed follicular thyroid cells...
- Kellie S, Craggs G, Bird I, Jones G. The tyrosine phosphatase DEP-1 induces cytoskeletal rearrangements, aberrant cell-substratum interactions and a reduction in cell proliferation. J Cell Sci. 2004;117:609-18 pubmed..These results demonstrate that DEP-1 is a negative regulator of cell proliferation, cell-substratum contacts, motility and chemotaxis in fibroblasts. ..
- Singh D, Lampe P. Identification of connexin-43 interacting proteins. Cell Commun Adhes. 2003;10:215-20 pubmed..Further in vitro/in vivo analysis of these interacting proteins will help in our understanding of the global role of connexins in regulating development, cell metabolism and growth. ..
- Petermann A, Haase D, Wetzel A, Balavenkatraman K, Tenev T, Gührs K, et al. Loss of the protein-tyrosine phosphatase DEP-1/PTPRJ drives meningioma cell motility. Brain Pathol. 2011;21:405-18 pubmed publisherDEP-1/PTPRJ is a transmembrane protein-tyrosine phosphatase which has been proposed as a suppressor of epithelial tumors...
- Hinojos C, Boerwinkle E, Fornage M, Doris P. Combined genealogical, mapping, and expression approaches to identify spontaneously hypertensive rat hypertension candidate genes. Hypertension. 2005;45:698-704 pubmed..The present approach identifies a number of genes that may influence blood pressure in SHR by virtue of allelic effects on gene expression. ..
- Senis Y, Tomlinson M, Ellison S, Mazharian A, Lim J, Zhao Y, et al. The tyrosine phosphatase CD148 is an essential positive regulator of platelet activation and thrombosis. Blood. 2009;113:4942-54 pubmed publisher..G protein-coupled receptor responses to thrombin and other agonists were also marginally reduced. These results highlight CD148 as a global regulator of platelet activation and a novel antithrombotic drug target. ..
- de la Fuente García M, Nicolas J, Freed J, Palou E, Thomas A, Vilella R, et al. CD148 is a membrane protein tyrosine phosphatase present in all hematopoietic lineages and is involved in signal transduction on lymphocytes. Blood. 1998;91:2800-9 pubmed..In conclusion, the data presented show that CD148 corresponds to a previously described protein tyrosine phosphatase HPTP-eta/DEP-1 and that this molecule is involved in signal transduction in lymphocytes. ..