| http://purl.uniprot.org/citations/19435816 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/19435816 | http://www.w3.org/2000/01/rdf-schema#comment | "Wild-type p53-induced phosphatase (Wip1) is a serine/threonine phosphatase induced by DNA-damaging agents. This enzyme dephosphorylates several cell cycle regulating proteins, including p53, p38 mitogen-activated protein kinase, Chk1, and Chk2, resulting in negative feedback regulation of p38-p53 signaling after damage repair. Moreover, the Wip1 gene may be amplified or overexpressed, especially in hormone-regulated organs, and Wip1 gene amplification has been correlated with poor prognosis in hormone-related malignancies, including ovarian cancers. We therefore investigated the link between estrogen signaling and Wip1 expression. We identified seven putative estrogen response elements within 3 kb of the Wip1 promoter. We also found that estradiol (E(2)) treatment produced a 3-fold increase in endogenous Wip1 mRNA and protein expression in MCF7 cells. Direct binding of estrogen receptor (ER)alpha to the Wip1 promoter after E(2) treatment was confirmed by a chromatin immunoprecipitation assay using ERalpha antibody and an electrophoretic mobility shift assay. Wip1 overexpression induced by adenovirus and E(2) facilitated the proliferation of serum-starved ZR-75-1 cells, with cell proliferation induced by overexpressed Wip1 approximately 25% higher than that induced by E(2). Wip1 phosphatase activity was essential for cell cycle progression. Wip1 stimulated the transcriptional activity of its own promoter through E(2)-ERalpha signaling. In addition, Wip1 overexpression induced Rb phosphorylation during cancer cell proliferation. These results indicate that Wip1 up-regulation is important in the pathogenesis of p53(+) and ER(+) breast cancer through the inactivation of p53 by dephosphorylation and the amplification of subsequent estrogenic effects through the E(2)-ERalpha-Wip1 pathway."xsd:string |
| http://purl.uniprot.org/citations/19435816 | http://purl.org/dc/terms/identifier | "doi:10.1158/1541-7786.mcr-08-0247"xsd:string |
| http://purl.uniprot.org/citations/19435816 | http://purl.uniprot.org/core/author | "Song J.Y."xsd:string |
| http://purl.uniprot.org/citations/19435816 | http://purl.uniprot.org/core/author | "Park J.Y."xsd:string |
| http://purl.uniprot.org/citations/19435816 | http://purl.uniprot.org/core/author | "Choi J."xsd:string |
| http://purl.uniprot.org/citations/19435816 | http://purl.uniprot.org/core/author | "Han H.S."xsd:string |
| http://purl.uniprot.org/citations/19435816 | http://purl.uniprot.org/core/author | "Jang S.J."xsd:string |
| http://purl.uniprot.org/citations/19435816 | http://purl.uniprot.org/core/author | "Yu E."xsd:string |
| http://purl.uniprot.org/citations/19435816 | http://purl.uniprot.org/core/date | "2009"xsd:gYear |
| http://purl.uniprot.org/citations/19435816 | http://purl.uniprot.org/core/name | "Mol Cancer Res"xsd:string |
| http://purl.uniprot.org/citations/19435816 | http://purl.uniprot.org/core/pages | "713-723"xsd:string |
| http://purl.uniprot.org/citations/19435816 | http://purl.uniprot.org/core/title | "The estrogen receptor alpha pathway induces oncogenic Wip1 phosphatase gene expression."xsd:string |
| http://purl.uniprot.org/citations/19435816 | http://purl.uniprot.org/core/volume | "7"xsd:string |
| http://purl.uniprot.org/citations/19435816 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/19435816 |
| http://purl.uniprot.org/citations/19435816 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/19435816 |
| http://purl.uniprot.org/uniprot/#_A0A125SXW0-mappedCitation-19435816 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/19435816 |
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