| http://purl.uniprot.org/citations/25609089 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/25609089 | http://www.w3.org/2000/01/rdf-schema#comment | "Receptor protein tyrosine phosphatase-κ (PTPRK) specifically and directly dephosphorylates epidermal growth factor receptor (EGFR), thereby limiting EGFR function in primary human keratinocytes. PTPRK expression is increased by the TGF-β/Smad3 pathway and cell-cell contact. Because the Notch receptor pathway is responsive to cell-cell contact and regulates keratinocyte growth and differentiation, we investigated the interplay between Notch and TGF-β pathways in regulation of PTPRK expression in human keratinocytes. Suppression of Notch signaling by γ-secretase inhibitors substantially reduced cell contact induction of PTPRK gene expression. In sparse keratinocyte cultures, addition of soluble Notch-activating ligand jagged one peptide (Jag1) induced PTPRK. Of interest, cell contact-induced expression of TGF-β1 and TGF-β receptor inhibitor SB431542 inhibited contact-induced expression of PTPRK. Furthermore, inhibition of Notch signaling, via knockdown of Notch1 or by γ-secretase inhibitors, significantly reduced TGF-β-induced PTPRK gene expression, indicating that Notch and TGF-β pathways function together to regulate PTPRK. Of importance, the combination of Jag1 plus TGF-β results in greater PTPRK expression and lower EGFR tyrosine phosphorylation than either ligand alone. These data indicate that Notch and TGF-β act in concert to stimulate induction of PTPRK, which suppresses EGFR activation in human keratinocytes."xsd:string |
| http://purl.uniprot.org/citations/25609089 | http://purl.org/dc/terms/identifier | "doi:10.1091/mbc.e14-12-1591"xsd:string |
| http://purl.uniprot.org/citations/25609089 | http://purl.uniprot.org/core/author | "Zhou J."xsd:string |
| http://purl.uniprot.org/citations/25609089 | http://purl.uniprot.org/core/author | "Xu Y."xsd:string |
| http://purl.uniprot.org/citations/25609089 | http://purl.uniprot.org/core/author | "Xue S."xsd:string |
| http://purl.uniprot.org/citations/25609089 | http://purl.uniprot.org/core/author | "Voorhees J.J."xsd:string |
| http://purl.uniprot.org/citations/25609089 | http://purl.uniprot.org/core/author | "Fisher G.J."xsd:string |
| http://purl.uniprot.org/citations/25609089 | http://purl.uniprot.org/core/date | "2015"xsd:gYear |
| http://purl.uniprot.org/citations/25609089 | http://purl.uniprot.org/core/name | "Mol Biol Cell"xsd:string |
| http://purl.uniprot.org/citations/25609089 | http://purl.uniprot.org/core/pages | "1199-1206"xsd:string |
| http://purl.uniprot.org/citations/25609089 | http://purl.uniprot.org/core/title | "Notch and TGF-beta pathways cooperatively regulate receptor protein tyrosine phosphatase-kappa (PTPRK) gene expression in human primary keratinocytes."xsd:string |
| http://purl.uniprot.org/citations/25609089 | http://purl.uniprot.org/core/volume | "26"xsd:string |
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