PTPRJ (protein tyrosine phosphatase, receptor type, J)

Multiple transcript variants encoding different isoforms have been found for this gene. Three transcripts are described in Ensembl (ID: ENSG00000149177). The first (ENST00000418331) represents the longer isoform and encodes a protein that consists of an extracellular fibronectin type 3 domain and a cytosolic catalytic domain. The second isoform (ENST00000440289) has multiple differences in the presence and absence of exons at its 3' end, compared to the first isoform. These differences produce a unique 3' UTR and the encoded protein is shorter and consists of the extracellular fibronectin type 3 domain without the cytosolic catalytic region. The third transcript (ENST00000278456) has the same length as the first, but it encodes a truncated protein, that consists of fibronectin type 3 domains. Only the first two isoforms are members of the human CCDS set and have been described in NCBI (IDs: NM_001098503.1, NM_001098503.1). The cDNA encoding PTPRJ/DEP-1 was isolated from a HeLa cell library (Ostman et al., 1994). The expression level and the activity of DEP-1 increase with cell density. This increase occurs gradually with increasing cell contact and is initiated before saturation cell density is reached. These observations suggest that DEP-1 may contribute to the mechanism of contact inhibition of cell growth.

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[2]  C. Croce,et al.  Role of PTPRJ genotype in papillary thyroid carcinoma risk. , 2010, Endocrine-related cancer.

[3]  I. Tomlinson,et al.  Germline epigenetic silencing of the tumor suppressor gene PTPRJ in early-onset familial colorectal cancer. , 2010, Gastroenterology.

[4]  Ziqiu Wang,et al.  Involvement of receptor tyrosine phosphatase DEP‐1 mediated PI3K‐cofilin signaling pathway in Sorafenib‐induced cytoskeletal rearrangement in hepatoma cells , 2010, Journal of cellular physiology.

[5]  Joshua F. McMichael,et al.  Genome Remodeling in a Basal-like Breast Cancer Metastasis and Xenograft , 2010, Nature.

[6]  I. Prior,et al.  Phosphatome profiling reveals PTPN2, PTPRJ and PTEN as potent negative regulators of PKB/Akt activation in Ras-mutated cancer cells. , 2010, The Biochemical journal.

[7]  S. Toyooka,et al.  Missense polymorphisms of PTPRJ and PTPN13 genes affect susceptibility to a variety of human cancers , 2010, Journal of Cancer Research and Clinical Oncology.

[8]  P. Mischel,et al.  An Unbiased Screen Identifies DEP-1 Tumor Suppressor as a Phosphatase Controlling EGFR Endocytosis , 2009, Current Biology.

[9]  L. Castagnoli,et al.  Tumor Suppressor Density-enhanced Phosphatase-1 (DEP-1) Inhibits the RAS Pathway by Direct Dephosphorylation of ERK1/2 Kinases* , 2009, The Journal of Biological Chemistry.

[10]  Wen Hwa Lee,et al.  Large-Scale Structural Analysis of the Classical Human Protein Tyrosine Phosphatome , 2009, Cell.

[11]  Xinning Jiang,et al.  Glycoproteomics analysis of human liver tissue by combination of multiple enzyme digestion and hydrazide chemistry. , 2009, Journal of proteome research.

[12]  Kathleen M Spring,et al.  New Role for the Protein Tyrosine Phosphatase DEP-1 in Akt Activation and Endothelial Cell Survival , 2008, Molecular and Cellular Biology.

[13]  F. Orsenigo,et al.  The role of adherens junctions and VE-cadherin in the control of vascular permeability , 2008, Journal of Cell Science.

[14]  R. Roberts,et al.  The tyrosine phosphatase CD148 interacts with the p85 regulatory subunit of phosphoinositide 3-kinase. , 2008, The Biochemical journal.

[15]  A. Weiss,et al.  Structurally distinct phosphatases CD45 and CD148 both regulate B cell and macrophage immunoreceptor signaling. , 2008, Immunity.

[16]  M. Lampugnani,et al.  The control of endothelial cell functions by adherens junctions. , 2007, Novartis Foundation symposium.

[17]  A. Östman,et al.  DEP-1 protein tyrosine phosphatase inhibits proliferation and migration of colon carcinoma cells and is upregulated by protective nutrients , 2006, Oncogene.

[18]  F. Orsenigo,et al.  Vascular endothelial cadherin controls VEGFR-2 internalization and signaling from intracellular compartments , 2006, The Journal of cell biology.

[19]  G. Viglietto,et al.  The receptor-type protein tyrosine phosphatase J antagonizes the biochemical and biological effects of RET-derived oncoproteins. , 2006, Cancer research.

[20]  J. Shield,et al.  Sensori-Neural Deafness and Hypothyroidism: Autoimmunity Causing ‘Pseudo-Pendred Syndrome’ , 2006, Hormone Research in Paediatrics.

[21]  Ronald J Moore,et al.  Human plasma N-glycoproteome analysis by immunoaffinity subtraction, hydrazide chemistry, and mass spectrometry. , 2005, Journal of proteome research.

[22]  D. Engelman,et al.  Transmembrane homodimerization of receptor‐like protein tyrosine phosphatases , 2005, FEBS letters.

[23]  A. Fusco,et al.  The tyrosine phosphatase PTPRJ/DEP-1 genotype affects thyroid carcinogenesis , 2004, Oncogene.

[24]  A. Weiss,et al.  Regulated Expression of the Receptor-Like Tyrosine Phosphatase CD148 on Hemopoietic Cells1 , 2004, The Journal of Immunology.

[25]  Tom van Wezel,et al.  Five new mouse susceptibility to colon cancer loci, Scc11–Scc15 , 2003, Oncogene.

[26]  A. Weiss,et al.  The tyrosine phosphatase CD148 is excluded from the immunologic synapse and down-regulates prolonged T cell signaling , 2003, The Journal of cell biology.

[27]  A. Östman,et al.  The protein-tyrosine phosphatase DEP-1 modulates growth factor-stimulated cell migration and cell–matrix adhesion , 2003, Oncogene.

[28]  G. Meijer,et al.  LOH of PTPRJ occurs early in colorectal cancer and is associated with chromosomal loss of 18q12–21 , 2003, Oncogene.

[29]  Paul A. Fleming,et al.  A Mutant Receptor Tyrosine Phosphatase, CD148, Causes Defects in Vascular Development , 2003, Molecular and Cellular Biology.

[30]  N. Tonks,et al.  Hepatocyte Growth Factor Receptor Tyrosine Kinase Met Is a Substrate of the Receptor Protein-tyrosine Phosphatase DEP-1* , 2003, The Journal of Biological Chemistry.

[31]  B. Jallal,et al.  The transmembrane receptor protein tyrosine phosphatase DEP1 interacts with p120ctn , 2002, Oncogene.

[32]  M. Cilli,et al.  Autoantibodies to inner ear and endothelial antigens in Cogan's syndrome , 2002, The Lancet.

[33]  Cestmir Vlcek,et al.  Ptprj is a candidate for the mouse colon-cancer susceptibility locus Scc1 and is frequently deleted in human cancers , 2002, Nature Genetics.

[34]  A. Östman,et al.  An extracellular ligand increases the specific activity of the receptor-like protein tyrosine phosphatase DEP-1 , 2001, Oncogene.

[35]  S. Tangye,et al.  Protein Tyrosine Phosphatase CD148-Mediated Inhibition of T-Cell Receptor Signal Transduction Is Associated with Reduced LAT and Phospholipase Cγ1 Phosphorylation , 2001, Molecular and Cellular Biology.

[36]  G. Viglietto,et al.  Rat Protein Tyrosine Phosphatase η Suppresses the Neoplastic Phenotype of Retrovirally Transformed Thyroid Cells through the Stabilization of p27Kip1 , 2000, Molecular and Cellular Biology.

[37]  R. Vilella,et al.  Site-selective Dephosphorylation of the Platelet-derived Growth Factor β-Receptor by the Receptor-like Protein-tyrosine Phosphatase DEP-1* , 2000, The Journal of Biological Chemistry.

[38]  F. Autschbach,et al.  Expression of the membrane protein tyrosine phosphatase CD148 in human tissues. , 1999, Tissue antigens.

[39]  S. Tangye,et al.  Negative regulation of human T cell activation by the receptor-type protein tyrosine phosphatase CD148. , 1998, Journal of immunology.

[40]  Y. Yazaki,et al.  Molecular cloning, characterization, and chromosomal localization of a novel protein-tyrosine phosphatase, HPTP eta. , 1994, Blood.

[41]  N. Tonks,et al.  Expression of DEP-1, a receptor-like protein-tyrosine-phosphatase, is enhanced with increasing cell density. , 1994, Proceedings of the National Academy of Sciences of the United States of America.

[42]  R. Roberts,et al.  The tyrosine phosphatase CD 148 interacts with the p 85 regulatory subunit of phosphoinositide 3-kinase , 2008 .

[43]  M. Lampugnani,et al.  Adherens junctions in endothelial cells regulate vessel maintenance and angiogenesis. , 2007, Thrombosis research.