Database for Annotation, Visualization and Integrated Discovery 2.1
National Institute of Allergy and Infectious Disease
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protein tyrosine phosphatase, receptor type J(PTPRJ) protein tyrosine phosphatase, receptor type J(PTPRJ) Related Genes Homo sapiens
CYTOBAND 11p11.2,
GENERIF_SUMMARY In this paper, frequent deletion of PTPRJ is shown in human colon, lung, and breast cancers., This protein is frequently deleted in human breast cancers., CD148 and CD27 are expressed in a wide range of B cell non-Hodgkin's lymphomas and do not serve to distinguish between neoplastic cells of naive and memory B cell derivation, DEP-1 is a negative regulator of cell proliferation, cell-substratum contacts, motility and chemotaxis in fibroblasts, propose that the expression and activation of DEP-1/PTPeta is required for somatostatin inhibition of glioma proliferation, A candidate tumor suppressor gene because its expression was blocked in rat and human thyroid transformed cells, and its restoration reverted their neoplastic phenotype., genotypic profile of PTPRJ affects susceptibility to thyroid carcinomas, loss involved in thyroid carcinogenesis, single nucleotide polymorphisms in protein tyrosine phosphatase receptor type J is associated with breast cancer, Male, dizygotic twins were diagnosed with sensori-neural deafness at ages 5 and 21 months and later developed hypothyroidism at ages 24 and 28 months, respectively. Analysis for anti-DEP-1/CD148 autoantibodies described in Cogan syndrome proved positive., Chemoprotective nutrients elevated transcription of endogenous DEP-1 mRNA & expression of DEP-1 protein. Upregulation of DEP-1 expression & inhibition of cell growth & migration may be a previously unrecognized mechanism of chemoprevention by nutrients., Findings identify RET as a novel substrate of PTPRJ and suggest that PTPRJ expression levels may affect tumor phenotype associated with RET/PTC1 and RET(C634R) mutants., These results demonstrate that CD148 may interact with and dephosphorylate p85 when it is phosphorylated and modulate the magnitude of phosphoinositide 3-kinase activity., The translation of the region between AUG(191) and AUG(356) inhibits the overall expression of PTPRJ mRNA., No significant evidence for the A1176C allele of PTPRJ or previously described haplotypes of tagSNPs in PTPRJ on CRC risk., DEP-1 is a positive regulator of VEGF-mediated Src and Akt activation and endothelial cell survival., The intact structure of the eighth fibronectin domain of PTPRJ is critical for its localization in plasma membrane and biological function., DEP-1 can modify the phosphorylation state of tight junction proteins and play a role in regulating permeability., CD148 may have a role in mantle cell lymphoma, DEP-1 inhibits the RAS pathway by direct dephosphorylation of ERK1/2 kinases, PTPRJ SNPs were found to influence susceptibility to a wide spectrum of cancers., DEP-1 is a tumor suppressor that dephosphorylates and thereby stabilizes EGFR by hampering its ability to associate with the CBL-GRB2 ubiquitin ligase complex., Data reveal PTPN2, PTPRJ and PTEN as potent regulators of Akt signalling which contribute to ameliorating the consequences of oncogenic K-Ras activity., Therefore, the results reported here show that the homozygous genotype for Asp872 of PTPRJ is associated with an increased risk to develop papillary thyroid carcinoma., PTPRJ is a candidate colorectal cancer susceptibility gene, We propose that positive regulation of adhesion signaling by DEP-1 is involved in inhibition of meningioma cell motility, and possibly tumor invasiveness., DEP-1 is negatively regulating FLT3 signaling activity and that its loss may contribute to but is not sufficient for leukemogenic cell transformation., 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, differential effects of CD148 in T cells and other leukocyte subsets, Here the protein tyrosine phosphatase receptor CD148 is shown to be a key intermediary in cell adhesion to S2ED, with downstream beta1 integrin-mediated adhesion and cytoskeletal organization, These findings provide evidence that CD148 functions as a receptor for TSP1 and mediates its inhibition of cell growth., DEP-1 oxidation is a novel event contributing to cell transformation by FLT3 ITD., Data indicate that miR-328 regulated PTPRJ expression, and suggest that the interaction of miR-328 with PTPRJ is responsible for miR-328-dependent increase of epithelial cell proliferation., CD148 polymorphisms affect platelet activation and probably exert a protective effect on the risk of Heparin-induced thrombocytopenia in patients with antibodies to PF4/Heparin complexes., These data indicate that PTPRJ may regulate differentiation of normal mammary epithelia and that dysregulation of protein localisation may be associated with tumorigenesis., haplotypes in PTPRJ gene may play a role in susceptibility to Non-Hodgkin's lymphoma, by affecting activation of PTPRJ in these B-cell lymphomas., FLT3 is a bona fide substrate of DEP-1 and that interaction occurs mainly via an enzyme-substrate complex formation triggered by FLT3 ligand stimulation., Data indicate that CD148 is upregulated in macrophages and T cells in rheumatoid arthritis (RA) samples, and its activity is enhanced by treatment with tumour necrosis factor alpha (TNFalpha), and reduced by synovial fluid or oxidising conditions., our data support the notion of DEP-1 as positive functional regulator in vascular cerebral arteriogenesis, involving differential PDGF-B gene expression., Phosphorylation of T1318 is part of a regulatory mechanism that channels the activity of DEP-1 towards Src to allow its optimal activation and the promotion of endothelial cell permeability., CD148 tyrosine phosphatase promotes e-cadherin cell adhesion., The expression profiles of DEP1 and B2MG correlate with increased cell senescence and survival in breast cancer., C33A cells lacking PTPRJ had increased cell viability, growth, migration, G1-S transition, and 5-FU resistance. PTPRJ negatively regulated the JAK1/STAT3 pathway by decreasing phosphorylation levels of JAK1 and STAT3 and expression of downstream factors., The studies suggest induction of MMP-9 expression promoted by DEP-1 deficiency., Moderate expression of DEP-1 was associated with the increased relapse., the combination of CD200 and CD148 may have a potential differential diagnostic value in leukemic B-CLPDs, especially between CLL and MCL., These results demonstrated Ptprj as a physiological enzyme that attenuates insulin signalling in vivo, and indicate that an inhibitor of Ptprj may be an insulin-sensitizing agent.,
OMIM_DISEASE Colon cancer, somatic,
SP_COMMENT catalytic activity:Protein tyrosine phosphate + H(2)O = protein tyrosine + phosphate., disease:Defects in PTPRJ are found in cancers of colon, lung, and breast., function:May contribute to the mechanism of contact inhibition of cell growth., PTM:N- and O-glycosylated., similarity:Belongs to the protein-tyrosine phosphatase family. Receptor class 3 subfamily., similarity:Contains 1 tyrosine-protein phosphatase domain., similarity:Contains 9 fibronectin type-III domains.,