| pubmed-article:12874272 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:12874272 | lifeskim:mentions | umls-concept:C0262950 | lld:lifeskim |
| pubmed-article:12874272 | lifeskim:mentions | umls-concept:C0021467 | lld:lifeskim |
| pubmed-article:12874272 | lifeskim:mentions | umls-concept:C0162493 | lld:lifeskim |
| pubmed-article:12874272 | lifeskim:mentions | umls-concept:C1422622 | lld:lifeskim |
| pubmed-article:12874272 | lifeskim:mentions | umls-concept:C0021469 | lld:lifeskim |
| pubmed-article:12874272 | lifeskim:mentions | umls-concept:C1514873 | lld:lifeskim |
| pubmed-article:12874272 | pubmed:issue | 40 | lld:pubmed |
| pubmed-article:12874272 | pubmed:dateCreated | 2003-9-29 | lld:pubmed |
| pubmed-article:12874272 | pubmed:abstractText | Multiple co-repressors such as N-CoR/SMRT, mSin3, and the c-ski proto-oncogene product (c-Ski) mediate the transcriptional repression induced by Mad and the thyroid hormone receptor by recruiting the histone deacetylase complex. c-Ski also binds directly to Smad proteins, which are transcriptional activators in the transforming growth factor-beta (TGF-beta)/bone morphogenetic protein (BMP) signaling pathways, and inhibits TGF-beta/BMP-induced transcriptional activation. However, it remains unknown whether other co-repressor(s) are also involved with Ski in the negative regulation of the TGF-beta/BMP signaling pathways. Here, we report that the co-repressor homeodomain-interacting protein kinase 2 (HIPK2) directly binds to both c-Ski and Smad1. HIPK2 efficiently inhibited Smad1/4-induced transcription from the Smad site-containing promoter. A dominant negative form of HIPK2, in which the ATP binding motif in the kinase domain and the putative phosphorylation sites were mutated, enhanced Smad1/4-dependent transcription and the BMP-induced expression of alkaline phosphatase. Furthermore, the c-Ski-induced inhibition of the Smad1/4-dependent transcription was suppressed by a dominant negative form of HIPK2. The HIPK2 co-repressor activity may be regulated by an uncharacterized HIPK2 kinase. These results indicate that HIPK2, together with c-Ski, plays an important role in the negative regulation of BMP-induced transcriptional activation. | lld:pubmed |
| pubmed-article:12874272 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:12874272 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:12874272 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:12874272 | pubmed:month | Oct | lld:pubmed |
| pubmed-article:12874272 | pubmed:issn | 0021-9258 | lld:pubmed |
| pubmed-article:12874272 | pubmed:author | pubmed-author:HaradaJunJ | lld:pubmed |
| pubmed-article:12874272 | pubmed:author | pubmed-author:IshiiShunsuke... | lld:pubmed |
| pubmed-article:12874272 | pubmed:author | pubmed-author:NomuraTeruaki... | lld:pubmed |
| pubmed-article:12874272 | pubmed:author | pubmed-author:KhanMd... | lld:pubmed |
| pubmed-article:12874272 | pubmed:author | pubmed-author:KokuraKenjiK | lld:pubmed |
| pubmed-article:12874272 | pubmed:author | pubmed-author:Kanei-IshiiCh... | lld:pubmed |
| pubmed-article:12874272 | pubmed:author | pubmed-author:KimYongsokY | lld:pubmed |
| pubmed-article:12874272 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:12874272 | pubmed:day | 3 | lld:pubmed |
| pubmed-article:12874272 | pubmed:volume | 278 | lld:pubmed |
| pubmed-article:12874272 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:12874272 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:12874272 | pubmed:pagination | 38998-9005 | lld:pubmed |
| pubmed-article:12874272 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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| pubmed-article:12874272 | pubmed:year | 2003 | lld:pubmed |
| pubmed-article:12874272 | pubmed:articleTitle | Requirement of the co-repressor homeodomain-interacting protein kinase 2 for ski-mediated inhibition of bone morphogenetic protein-induced transcriptional activation. | lld:pubmed |
| pubmed-article:12874272 | pubmed:affiliation | Laboratory of Molecular Genetics, RIKEN Tsukuba Institute, 3-1-1 Koyadai, Tsukuba, Ibaraki 305-0074, Japan. | lld:pubmed |
| pubmed-article:12874272 | pubmed:publicationType | Journal Article | lld:pubmed |
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