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http://purl.uniprot.org/citations/11773439http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/11773439http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/11773439http://www.w3.org/2000/01/rdf-schema#comment"In the present study we examined involvement of nuclear protein tyrosine phosphatase TC-PTP in PRL-mediated signaling. TC-PTP could dephosphorylate signal transducer and activator of transcription 5a (STAT5a) and STAT5b, but the apparent dephosphorylation activity of TC-PTP was weaker than that of cytosolic PTP1B 30 min after PRL stimulation in transfected COS-7 cells, whereas both STAT5a and STAT5b were dephosphorylated to the same extent by recombinant TC-PTP and PTP1B in vitro. Tyrosine-phosphorylated STAT5 was coimmunoprecipitated with substrate trapping mutants of TC-PTP, suggesting that STAT5 is a specific substrate of TC-PTP. These observations were further extended in mammary epithelial COMMA-1D cells stably expressing TC-PTP. A time-course study revealed that dephosphorylation of STAT5 by TC-PTP was delayed compared with that by cytosolic PTP1B due to nuclear localization of TC-PTP throughout PRL stimulation in mammary epithelial cells. Endogenous beta-casein gene expression and beta-casein gene promoter activation in COS-7 cells were largely suppressed by TC-PTP wild type as well as catalytically inactive mutants, suggesting that stable complexes formed between STAT5 and TC-PTP in the nucleus. Taken together, we conclude that TC-PTP is catalytically competent with respect to dephosphorylation and deactivation of PRL-activated STAT5 in the nucleus."xsd:string
http://purl.uniprot.org/citations/11773439http://purl.org/dc/terms/identifier"doi:10.1210/mend.16.1.0761"xsd:string
http://purl.uniprot.org/citations/11773439http://purl.org/dc/terms/identifier"doi:10.1210/mend.16.1.0761"xsd:string
http://purl.uniprot.org/citations/11773439http://purl.uniprot.org/core/author"Aoki N."xsd:string
http://purl.uniprot.org/citations/11773439http://purl.uniprot.org/core/author"Aoki N."xsd:string
http://purl.uniprot.org/citations/11773439http://purl.uniprot.org/core/author"Matsuda T."xsd:string
http://purl.uniprot.org/citations/11773439http://purl.uniprot.org/core/author"Matsuda T."xsd:string
http://purl.uniprot.org/citations/11773439http://purl.uniprot.org/core/date"2002"xsd:gYear
http://purl.uniprot.org/citations/11773439http://purl.uniprot.org/core/date"2002"xsd:gYear
http://purl.uniprot.org/citations/11773439http://purl.uniprot.org/core/name"Mol. Endocrinol."xsd:string
http://purl.uniprot.org/citations/11773439http://purl.uniprot.org/core/name"Mol. Endocrinol."xsd:string
http://purl.uniprot.org/citations/11773439http://purl.uniprot.org/core/pages"58-69"xsd:string
http://purl.uniprot.org/citations/11773439http://purl.uniprot.org/core/pages"58-69"xsd:string
http://purl.uniprot.org/citations/11773439http://purl.uniprot.org/core/title"A nuclear protein tyrosine phosphatase TC-PTP is a potential negative regulator of the PRL-mediated signaling pathway: dephosphorylation and deactivation of signal transducer and activator of transcription 5a and 5b by TC-PTP in nucleus."xsd:string
http://purl.uniprot.org/citations/11773439http://purl.uniprot.org/core/title"A nuclear protein tyrosine phosphatase TC-PTP is a potential negative regulator of the PRL-mediated signaling pathway: dephosphorylation and deactivation of signal transducer and activator of transcription 5a and 5b by TC-PTP in nucleus."xsd:string
http://purl.uniprot.org/citations/11773439http://purl.uniprot.org/core/volume"16"xsd:string
http://purl.uniprot.org/citations/11773439http://purl.uniprot.org/core/volume"16"xsd:string
http://purl.uniprot.org/citations/11773439http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/11773439
http://purl.uniprot.org/citations/11773439http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/11773439
http://purl.uniprot.org/citations/11773439http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/11773439
http://purl.uniprot.org/citations/11773439http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/11773439
http://purl.uniprot.org/uniprot/P42229http://purl.uniprot.org/core/citationhttp://purl.uniprot.org/citations/11773439
http://purl.uniprot.org/uniprot/P42232http://purl.uniprot.org/core/citationhttp://purl.uniprot.org/citations/11773439