DC Field | Value | Language |
---|---|---|
dc.contributor.author | Tomita, Mariko | ko |
dc.contributor.author | Choe, Joonho | ko |
dc.contributor.author | Tsukazaki, Tomoo | ko |
dc.contributor.author | Mori, Naoki | ko |
dc.date.accessioned | 2013-03-06T03:02:58Z | - |
dc.date.available | 2013-03-06T03:02:58Z | - |
dc.date.created | 2012-02-06 | - |
dc.date.created | 2012-02-06 | - |
dc.date.issued | 2004-10 | - |
dc.identifier.citation | ONCOGENE, v.23, no.50, pp.8272 - 8281 | - |
dc.identifier.issn | 0950-9232 | - |
dc.identifier.uri | http://hdl.handle.net/10203/85625 | - |
dc.description.abstract | Kaposi's sarcoma (KS)-associated herpesvirus (KSHV) is involved in the pathogenesis of KS, primary effusion lymphoma, and multicentric Castleman's disease. K-bZIP, the protein encoded by the open reading frame K8 of KSHV, is a member of the basic region-leucine zipper family of transcription factors. We studied the mechanisms that underlie KSHV-induced oncogenesis by investigating whether K-bZIP perturbs signaling through transforming growth factor beta (TGF-beta), which inhibits proliferation of a wide range of cell types. K-bZIP repressed TGF-beta-induced, Smad-mediated transcriptional activity and antagonized the growth-inhibitory effects of TGF-beta. Since both K-bZIP and Smad are known to interact with CREB-binding protein (CBP), the effect of CBP on inhibition of Smad-mediated transcriptional activation by K-bZIP was examined. K-bZIP mutants, which lacked the CBP-binding site, could not repress TGF-beta-induced or Smad3-mediated transcriptional activity. Overexpression of CBP restored K-bZIP-induced inhibition of Smad3-mediated transcriptional activity. Competitive interaction studies showed that K-bZIP inhibited the interaction of Smad3 with CBP. These results suggest that K-bZIP, through its binding to CBP, disrupts TGF-beta signaling by interfering with the recruitment of CBP into transcription initiation complexes on TGF-beta-responsive elements. We propose a possibility that K-bZIP may contribute to oncogenesis through its ability to promote cell survival by repressing TGF-beta signaling. | - |
dc.language | English | - |
dc.publisher | NATURE PUBLISHING GROUP | - |
dc.subject | FACTOR-KAPPA-B | - |
dc.subject | MULTICENTRIC CASTLEMANS-DISEASE | - |
dc.subject | EPSTEIN-BARR-VIRUS | - |
dc.subject | TGF-BETA | - |
dc.subject | DNA-SEQUENCES | - |
dc.subject | TRANSCRIPTIONAL ACTIVATION | - |
dc.subject | COACTIVATORS CBP/P300 | - |
dc.subject | NUCLEAR INTEGRATION | - |
dc.subject | GENE-EXPRESSION | - |
dc.subject | SMAD PROTEINS | - |
dc.title | The Kaposis sarcoma-associated herpesvirus K-bZIP protein represses transforming growth factor beta signaling through interaction with CREB-binding protein | - |
dc.type | Article | - |
dc.identifier.wosid | 000224749500009 | - |
dc.identifier.scopusid | 2-s2.0-8844287585 | - |
dc.type.rims | ART | - |
dc.citation.volume | 23 | - |
dc.citation.issue | 50 | - |
dc.citation.beginningpage | 8272 | - |
dc.citation.endingpage | 8281 | - |
dc.citation.publicationname | ONCOGENE | - |
dc.identifier.doi | 10.1038/sj.onc.1208059 | - |
dc.contributor.localauthor | Choe, Joonho | - |
dc.contributor.nonIdAuthor | Tomita, Mariko | - |
dc.contributor.nonIdAuthor | Tsukazaki, Tomoo | - |
dc.contributor.nonIdAuthor | Mori, Naoki | - |
dc.type.journalArticle | Article | - |
dc.subject.keywordAuthor | KSHV | - |
dc.subject.keywordAuthor | K-bZIP | - |
dc.subject.keywordAuthor | TGF-beta | - |
dc.subject.keywordAuthor | Smad | - |
dc.subject.keywordAuthor | CBP | - |
dc.subject.keywordPlus | FACTOR-KAPPA-B | - |
dc.subject.keywordPlus | MULTICENTRIC CASTLEMANS-DISEASE | - |
dc.subject.keywordPlus | EPSTEIN-BARR-VIRUS | - |
dc.subject.keywordPlus | TGF-BETA | - |
dc.subject.keywordPlus | DNA-SEQUENCES | - |
dc.subject.keywordPlus | TRANSCRIPTIONAL ACTIVATION | - |
dc.subject.keywordPlus | COACTIVATORS CBP/P300 | - |
dc.subject.keywordPlus | NUCLEAR INTEGRATION | - |
dc.subject.keywordPlus | GENE-EXPRESSION | - |
dc.subject.keywordPlus | SMAD PROTEINS | - |
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