pubmed-article:11387330 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:11387330 | lifeskim:mentions | umls-concept:C0006104 | lld:lifeskim |
pubmed-article:11387330 | lifeskim:mentions | umls-concept:C0009015 | lld:lifeskim |
pubmed-article:11387330 | lifeskim:mentions | umls-concept:C0037083 | lld:lifeskim |
pubmed-article:11387330 | lifeskim:mentions | umls-concept:C0040690 | lld:lifeskim |
pubmed-article:11387330 | lifeskim:mentions | umls-concept:C0205245 | lld:lifeskim |
pubmed-article:11387330 | lifeskim:mentions | umls-concept:C0033713 | lld:lifeskim |
pubmed-article:11387330 | lifeskim:mentions | umls-concept:C1710082 | lld:lifeskim |
pubmed-article:11387330 | lifeskim:mentions | umls-concept:C0231491 | lld:lifeskim |
pubmed-article:11387330 | pubmed:issue | 32 | lld:pubmed |
pubmed-article:11387330 | pubmed:dateCreated | 2001-8-6 | lld:pubmed |
pubmed-article:11387330 | pubmed:abstractText | Using the plasminogen activator inhibitor (PAI) promoter to drive the expression of a reporter gene (mouse CD2), we devised a system to clone negative regulators of the transforming growth factor-beta (TGF-beta) signaling pathway. We infected a TGF-beta-responsive cell line (MvLu1) with a retroviral cDNA library, selecting by fluorescence-activated cell sorter single cells displaying low PAI promoter activity in response to TGF-beta. Using this strategy we cloned the proto-oncogene brain factor-1 (BF-1). BF-1 represses the PAI promoter in part by associating with both unphosphorylated Smad3 (in the cytoplasm) and phosphorylated Smad3 (in the nucleus), thus preventing its binding to DNA. BF-1 also associates with Smad1, -2, and -4; the Smad MH2 domain binds to BF-1, and the C-terminal segment of BF-1 is uniquely and solely required for binding to Smads. Further, BF-1 represses another TGF-beta-induced promoter (p15), it up-regulates a TGF-beta-repressed promoter (Cyclin A), and it reverses the growth arrest caused by TGF-beta. Our results suggest that BF-1 is a general inhibitor of TGF-beta signaling and as such may play a key role during brain development. | lld:pubmed |
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pubmed-article:11387330 | pubmed:language | eng | lld:pubmed |
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pubmed-article:11387330 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:11387330 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:11387330 | pubmed:month | Aug | lld:pubmed |
pubmed-article:11387330 | pubmed:issn | 0021-9258 | lld:pubmed |
pubmed-article:11387330 | pubmed:author | pubmed-author:LodishH FHF | lld:pubmed |
pubmed-article:11387330 | pubmed:author | pubmed-author:RodriguezCC | lld:pubmed |
pubmed-article:11387330 | pubmed:author | pubmed-author:McKeeAA | lld:pubmed |
pubmed-article:11387330 | pubmed:author | pubmed-author:HuangL JLJ | lld:pubmed |
pubmed-article:11387330 | pubmed:author | pubmed-author:XiaoZZ | lld:pubmed |
pubmed-article:11387330 | pubmed:author | pubmed-author:SonJ KJK | lld:pubmed |
pubmed-article:11387330 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:11387330 | pubmed:day | 10 | lld:pubmed |
pubmed-article:11387330 | pubmed:volume | 276 | lld:pubmed |
pubmed-article:11387330 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:11387330 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:11387330 | pubmed:pagination | 30224-30 | lld:pubmed |
pubmed-article:11387330 | pubmed:dateRevised | 2008-11-21 | lld:pubmed |
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pubmed-article:11387330 | pubmed:year | 2001 | lld:pubmed |
pubmed-article:11387330 | pubmed:articleTitle | Functional cloning of the proto-oncogene brain factor-1 (BF-1) as a Smad-binding antagonist of transforming growth factor-beta signaling. | lld:pubmed |
pubmed-article:11387330 | pubmed:affiliation | Whitehead Institute for Biomedical Research, 9 Cambridge Center, Cambridge, Massachusetts 02142, USA. | lld:pubmed |
pubmed-article:11387330 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:11387330 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
pubmed-article:11387330 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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