InnateDB: Systems Biology of the Innate Immune Response

Homo sapiens Protein: PTPRC

Summary

InnateDB Protein

IDBP-105615.7

Last Modified

2014-10-13 [Report errors or provide feedback]

Gene Symbol

PTPRC

Protein Name

protein tyrosine phosphatase, receptor type, C

Synonyms

B220; CD45; CD45R; GP180; L-CA; LCA; LY5; T200;

Species

Homo sapiens

Ensembl Protein

ENSP00000306782

InnateDB Gene

IDBG-105609 (PTPRC)

Protein Structure

UniProt Annotation

Function

Protein tyrosine-protein phosphatase required for T-cell activation through the antigen receptor. Acts as a positive regulator of T-cell coactivation upon binding to DPP4. The first PTPase domain has enzymatic activity, while the second one seems to affect the substrate specificity of the first one. Upon T-cell activation, recruits and dephosphorylates SKAP1 and FYN. Dephosphorylates LYN, and thereby modulates LYN activity (By similarity). {ECO:0000250}.

Subcellular Localization

Membrane {ECO:0000269PubMed:12676959}; Single-pass type I membrane protein {ECO:0000269PubMed:12676959}. Membrane raft {ECO:0000269PubMed:12676959}. Note=Colocalized with DPP4 in membrane rafts.

Disease Associations

Severe combined immunodeficiency autosomal recessive T- cell-negative/B-cell-positive/NK-cell-positive (T(-)B(+)NK(+) SCID) [MIM:608971]: A form of severe combined immunodeficiency (SCID), a genetically and clinically heterogeneous group of rare congenital disorders characterized by impairment of both humoral and cell-mediated immunity, leukopenia, and low or absent antibody levels. Patients present in infancy recurrent, persistent infections by opportunistic organisms. The common characteristic of all types of SCID is absence of T-cell-mediated cellular immunity due to a defect in T-cell development. {ECO:0000269PubMed:11145714}. Note=The disease is caused by mutations affecting the gene represented in this entry.Multiple sclerosis (MS) [MIM:126200]: A multifactorial, inflammatory, demyelinating disease of the central nervous system. Sclerotic lesions are characterized by perivascular infiltration of monocytes and lymphocytes and appear as indurated areas in pathologic specimens (sclerosis in plaques). The pathological mechanism is regarded as an autoimmune attack of the myelin sheath, mediated by both cellular and humoral immunity. Clinical manifestations include visual loss, extra-ocular movement disorders, paresthesias, loss of sensation, weakness, dysarthria, spasticity, ataxia and bladder dysfunction. Genetic and environmental factors influence susceptibility to the disease. {ECO:0000269PubMed:11101853}. Note=Disease susceptibility may be associated with variations affecting the gene represented in this entry.

Tissue Specificity

Comments

Interactions

Number of Interactions

This gene and/or its encoded proteins are associated with 72 experimentally validated interaction(s) in this database.
They are also associated with 8 interaction(s) predicted by orthology.

Experimentally validated
Total	72 [view]
Protein-Protein	72 [view]
Protein-DNA	0
Protein-RNA	0
DNA-DNA	0
RNA-RNA	0
DNA-RNA	0

Predicted by orthology
Total	8 [view]

Gene Ontology

Molecular Function

Accession	GO Term
GO:0004725	protein tyrosine phosphatase activity
GO:0005515	protein binding
GO:0016791	phosphatase activity

Biological Process

GO:0006470	protein dephosphorylation
GO:0016311	dephosphorylation
GO:0035335	peptidyl-tyrosine dephosphorylation
GO:0045087	innate immune response (InnateDB)
GO:0050852	T cell receptor signaling pathway

Cellular Component

Protein Structure and Domains

PDB ID

InterPro

IPR000242 Protein-tyrosine phosphatase, receptor/non-receptor type
IPR000387 Protein-tyrosine/Dual specificity phosphatase
IPR003595 Protein-tyrosine phosphatase, catalytic
IPR003961 Fibronectin, type III
IPR016335 Leukocyte common antigen
IPR024739 Protein tyrosine phosphatase, receptor type, N-terminal
IPR029021 Protein-tyrosine phosphatase-like

PFAM

PF00102
PF00041
PF01108
PF12567
PF12453

PRINTS

PR00700

PIRSF

PIRSF002004

SMART

SM00194
SM00404
SM00060

TIGRFAMs

Post-translational Modifications

Modification

Cross-References