Disease relevance of PTPRK

• We selected protein tyrosine phosphatase kappa (PTPkappa) as a model protein to validate this approach to the discovery of novel biomarkers in colon cancer [1].

High impact information on PTPRK

• Receptor tyrosine phosphatase R-PTP-kappa mediates homophilic binding [2].
• R-PTP-kappa-mediated intercellular adhesion does not require PTPase activity or posttranslational proteolytic cleavage of the R-PTP-kappa protein and is calcium independent [2].
• LOH was found at 1 or more loci at 6q22-23 in 19 samples (66%); furthermore, 18 of these samples shared a deletion in the same small ( approximately 140 kb) region flanked by D6S1030 and D6S1690, a region in which the human R-PTP-kappa gene (PTPRK) is reported to be located [3].
• We report here that receptor-type protein-tyrosine phosphatase-kappa (RPTP-kappa) dephosphorylates EGFR and thereby regulates its function in human keratinocytes [4].
• Identification of a mutated receptor-like protein tyrosine phosphatase kappa as a novel, class II HLA-restricted melanoma antigen [5].

Associations of PTPRK with chemical compounds

• We speculate that loss of the phosphatase function of PTPRK may activate as-yet-unidentified growth-promoting protein tyrosine kinases, which in turn contribute to the pathogenesis of EBV-positive HL [6].

Biological context of PTPRK

• Cytogenetical assignment and physical mapping of the human R-PTP-kappa gene (PTPRK) to the putative tumor suppressor gene region 6q22.2-q22.3 [7].
• We studied regulation of a receptor-type tyrosine phosphatase R-PTP-kappa gene expression in a human keratinocyte cell line, HaCaT [8].
• Identification of target proteins of N-acetylglucosaminyl transferase V in human colon cancer and implications of protein tyrosine phosphatase kappa in enhanced cancer cell migration [1].

Anatomical context of PTPRK

• By a genetic approach, a peptide derived from a mutated receptor-like protein tyrosine phosphatase kappa was identified as a novel HLA-DR10-restricted epitope for all the melanoma-specific CD4(+) T cell clones [5].

Regulatory relationships of PTPRK

• The TGF-beta 1-induced R-PTP-kappa mRNA expression was suppressed by sodium orthovanadate, a tyrosine phosphatase inhibitor, and H7, a serine/threonine kinase inhibitor, but not by genistein, a tyrosine kinase inhibitor [8].

Other interactions of PTPRK

• Taken together, these results suggest that TGF-beta 1 inhibits the human keratinocyte proliferation in vitro, possibly through induction of R-PTP-kappa gene expression [8].

Analytical, diagnostic and therapeutic context of PTPRK

• Reverse transcription-PCR analysis of the mRNA from 4 cases with 6q deletions confirmed loss of this gene, and loss of PTPRK expression was observed in 76% (22 of 29) of tumors with immunohistochemistry [3].

References