DC Field | Value | Language |
---|---|---|
dc.contributor.author | Min, S-H | ko |
dc.contributor.author | Kim, D. M. | ko |
dc.contributor.author | Heo, Y-S | ko |
dc.contributor.author | Kim, Y-I | ko |
dc.contributor.author | Kim, Ho Min | ko |
dc.contributor.author | Kim, J. | ko |
dc.contributor.author | Han, Y-M | ko |
dc.contributor.author | Kim, I-C | ko |
dc.contributor.author | Yoo, Ook-Joon | ko |
dc.date.accessioned | 2013-03-12T04:57:23Z | - |
dc.date.available | 2013-03-12T04:57:23Z | - |
dc.date.created | 2012-02-06 | - |
dc.date.created | 2012-02-06 | - |
dc.date.issued | 2009-01 | - |
dc.identifier.citation | ONCOGENE, v.28, no.4, pp.545 - 554 | - |
dc.identifier.issn | 0950-9232 | - |
dc.identifier.uri | http://hdl.handle.net/10203/101376 | - |
dc.description.abstract | Most of the p53 target genes, all except MDM2, COP1 and PIRH2, perform functions in apoptosis, differentiation and cell cycle arrest. The aforementioned oncogenes downregulate p53 through a negative feedback mechanism, and thus contribute to tumor development. In this study, we report a new p53 target, PRL-1, which is believed to be a significant regulator in the development and metastasis of a variety of cancer types. Phosphatase of regenerating liver 1 (PRL-1) overexpression reduced the levels of endogenous and exogenous p53 proteins, and inhibited p53-mediated apoptosis. On the other hand, the ablation of PRL-1 by small interfering RNA (siRNA) increased p53 protein levels. The p53 downregulation was mediated by p53 ubiquitination and subsequent proteasomal degradation. Furthermore, p53 ubiquitination by PRL-1 was achieved through two independent pathways, by inducing PIRH2 transcription and by inducing MDM2 phosphorylation through Akt signaling. In addition, we showed that the PRL-1 gene harbors a p53 response element in the first intron, and its transcription is regulated by the p53 protein. These findings imply that the new oncogenic p53 target, PRL-1, may contribute to tumor development by the downregulation of p53 by a negative feedback mechanism. | - |
dc.language | English | - |
dc.publisher | NATURE PUBLISHING GROUP | - |
dc.subject | TUMOR-SUPPRESSOR PROTEIN | - |
dc.subject | GENE-EXPRESSION | - |
dc.subject | TYROSINE PHOSPHATASES | - |
dc.subject | CANCER-CELLS | - |
dc.subject | GROWTH | - |
dc.subject | ACTIVATION | - |
dc.subject | METASTASIS | - |
dc.subject | INVASION | - |
dc.subject | PHOSPHORYLATION | - |
dc.subject | MDM2 | - |
dc.title | New p53 target, phosphatase of regenerating liver 1 (PRL-1) downregulates p53 | - |
dc.type | Article | - |
dc.identifier.wosid | 000262866500008 | - |
dc.identifier.scopusid | 2-s2.0-59149094764 | - |
dc.type.rims | ART | - |
dc.citation.volume | 28 | - |
dc.citation.issue | 4 | - |
dc.citation.beginningpage | 545 | - |
dc.citation.endingpage | 554 | - |
dc.citation.publicationname | ONCOGENE | - |
dc.contributor.localauthor | Kim, Ho Min | - |
dc.contributor.localauthor | Yoo, Ook-Joon | - |
dc.contributor.nonIdAuthor | Min, S-H | - |
dc.contributor.nonIdAuthor | Kim, D. M. | - |
dc.contributor.nonIdAuthor | Heo, Y-S | - |
dc.contributor.nonIdAuthor | Kim, Y-I | - |
dc.contributor.nonIdAuthor | Kim, J. | - |
dc.contributor.nonIdAuthor | Han, Y-M | - |
dc.contributor.nonIdAuthor | Kim, I-C | - |
dc.type.journalArticle | Article | - |
dc.subject.keywordAuthor | p53 target | - |
dc.subject.keywordAuthor | phosphatase of regenerating liver 1 | - |
dc.subject.keywordAuthor | PRL-1 | - |
dc.subject.keywordAuthor | EGR | - |
dc.subject.keywordAuthor | PI3K | - |
dc.subject.keywordPlus | TUMOR-SUPPRESSOR PROTEIN | - |
dc.subject.keywordPlus | GENE-EXPRESSION | - |
dc.subject.keywordPlus | TYROSINE PHOSPHATASES | - |
dc.subject.keywordPlus | CANCER-CELLS | - |
dc.subject.keywordPlus | GROWTH | - |
dc.subject.keywordPlus | ACTIVATION | - |
dc.subject.keywordPlus | METASTASIS | - |
dc.subject.keywordPlus | INVASION | - |
dc.subject.keywordPlus | PHOSPHORYLATION | - |
dc.subject.keywordPlus | MDM2 | - |
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