Go Annotations as Summary Text (Tabular View) (GO Graph)

GO curators for mouse genes have assigned the following annotations to the gene product of Ptprj. (This text reflects annotations as of Wednesday, August 14, 2013.)

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Summary from NCBI RefSeq

[Summary is not available for the mouse gene. This summary is for the human ortholog.] The protein encoded by this gene is a member of the protein tyrosine phosphatase (PTP) family. PTPs are known to be signaling molecules that regulate a variety of cellular processes, including cell growth, differentiation, mitotic cycle, and oncogenic transformation. This PTP possesses an extracellular region containing five fibronectin type III repeats, a single transmembrane region, and a single intracytoplasmic catalytic domain, and thus represents a receptor-type PTP. This protein is present in all hematopoietic lineages, and was shown to negatively regulate T cell receptor signaling possibly through interfering with the phosphorylation of Phospholipase C Gamma 1 and Linker for Activation of T Cells. This protein can also dephosphorylate the PDGF beta receptor, and may be involved in UV-induced signal transduction. Multiple transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Jul 2008]

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Summary text based on GO annotations supported by experimental evidence in mouse

• Researchers have inferred from direct assay, that the gene product of Ptprj
  • participates in the following biological processes:
    • negative regulation of cell migration ^[3]
    • negative regulation of MAP kinase activity ^[3]
    • negative regulation of platelet-derived growth factor receptor signaling pathway ^[3]
    • negative regulation of T cell receptor signaling pathway ^[4]
    • positive regulation of cell-matrix adhesion ^[3]
    • positive regulation of macrophage chemotaxis ^[1]
  • is located in the following cellular components:
    • immunological synapse ^[4]
    • plasma membrane ^[1]
    • ruffle membrane ^[1]
• Researchers have inferred, based on phenotypic analysis of mouse mutants, that the gene product of Ptprj
  • participates in the following biological processes:
    • blood coagulation ^[5]
    • heart development ^[6]
    • negative regulation of cell proliferation ^[2]
    • negative regulation of receptor activity ^[2]
    • positive regulation of platelet activation ^[5]
    • vasculogenesis ^[6]
  • performs the following molecular functions:
    • protein tyrosine phosphatase activity ^[2]

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Summary text based on GO annotations supported by experimental evidence in other organisms

• From comparative sequence analysis (see table for details), MGI curators have determined that the gene product of Ptprj:
  • participates in the following biological processes:
    • negative regulation of cell growth
    • negative regulation of cell migration
    • negative regulation of cell proliferation
    • negative regulation of epidermal growth factor receptor signaling pathway
    • negative regulation of MAP kinase activity
    • negative regulation of platelet-derived growth factor receptor signaling pathway
    • negative regulation of protein kinase B signaling cascade
    • negative regulation of T cell receptor signaling pathway
    • negative regulation of vascular permeability
    • peptidyl-tyrosine dephosphorylation
    • platelet-derived growth factor receptor signaling pathway
    • positive chemotaxis
    • positive regulation of cell adhesion
    • positive regulation of focal adhesion assembly
    • positive regulation of protein kinase B signaling cascade
    • regulation of cell adhesion
  • performs the following molecular functions:
    • beta-catenin binding
    • delta-catenin binding
    • gamma-catenin binding
    • mitogen-activated protein kinase binding
    • phosphatase activity
    • platelet-derived growth factor receptor binding
    • protein kinase binding
    • protein tyrosine phosphatase activity
  • is located in the following cellular components:
    • cell surface
    • cell-cell junction
    • immunological synapse
    • plasma membrane

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Summary text based on GO annotations supported by structural data

• Ptprj encodes a protein or proteins that contain the following InterPro domains: Fibronectin, type III, Immunoglobulin-like fold, Protein-tyrosine phosphatase, active site, Protein-tyrosine phosphatase, receptor/non-receptor type, Protein-tyrosine/Dual specificity phosphatase, indicating that the gene product:
  • participates in the following biological processes:
    • dephosphorylation
    • protein dephosphorylation

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Summary text for additional MGI annotations

• Automated translation to GO terms of SwissProt keywords that describe Ptprj indicates that it:
  • performs the following molecular functions:
    • hydrolase activity
    • phosphoprotein phosphatase activity
  • is located in the following cellular components:
    • cell junction
    • cell projection
    • integral to membrane
    • membrane

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References

1. Dave RK et al. (2009) CD148/DEP-1 association with areas of cytoskeletal organisation in macrophages. Exp Cell Res, 315:1734-44. (PubMed:19268662)
2. Grazia Lampugnani M et al. (2003) Contact inhibition of VEGF-induced proliferation requires vascular endothelial cadherin, beta-catenin, and the phosphatase DEP-1/CD148. J Cell Biol, 161:793-804. (PubMed:12771128)
3. Jandt E et al. (2003) The protein-tyrosine phosphatase DEP-1 modulates growth factor-stimulated cell migration and cell-matrix adhesion. Oncogene, 22:4175-85. (PubMed:12833140)
4. Lin J et al. (2003) The tyrosine phosphatase CD148 is excluded from the immunologic synapse and down-regulates prolonged T cell signaling. J Cell Biol, 162:673-82. (PubMed:12913111)
5. Senis YA et al. (2009) The tyrosine phosphatase CD148 is an essential positive regulator of platelet activation and thrombosis. Blood, 113:4942-54. (PubMed:19246339)
6. Takahashi T et al. (2003) A mutant receptor tyrosine phosphatase, CD148, causes defects in vascular development. Mol Cell Biol, 23:1817-31. (PubMed:12588999)

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Gene Ontology Evidence Code Abbreviations:

EXP Inferred from experiment

IC Inferred by curator

IDA Inferred from direct assay

IEA Inferred from electronic annotation

IGI Inferred from genetic interaction

IMP Inferred from mutant phenotype

IPI Inferred from physical interaction

ISS Inferred from sequence or structural similarity

ISO Inferred from sequence orthology

ISA Inferred from sequence alignment

ISM Inferred from sequence model

NAS Non-traceable author statement

ND No biological data available

RCA Reviewed computational analysis

TAS Traceable author statement

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