| pubmed-article:9228025 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:9228025 | lifeskim:mentions | umls-concept:C0085828 | lld:lifeskim |
| pubmed-article:9228025 | lifeskim:mentions | umls-concept:C1326912 | lld:lifeskim |
| pubmed-article:9228025 | lifeskim:mentions | umls-concept:C1512032 | lld:lifeskim |
| pubmed-article:9228025 | lifeskim:mentions | umls-concept:C1148673 | lld:lifeskim |
| pubmed-article:9228025 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
| pubmed-article:9228025 | pubmed:issue | 30 | lld:pubmed |
| pubmed-article:9228025 | pubmed:dateCreated | 1997-9-9 | lld:pubmed |
| pubmed-article:9228025 | pubmed:abstractText | We describe a dominant negative (DN) to activation protein-1 (AP1) that inhibits DNA binding in an equimolar competition. AP1 is a heterodimer of the oncogenes Fos and Jun, members of the bZIP family of transcription factors. The DN, termed A-Fos, consists of a newly designed acidic amphipathic protein sequence appended onto the N-terminus of the Fos leucine zipper, replacing the normal basic region critical for DNA binding. The acidic extension and the Jun basic region form a heterodimeric coiled coil structure that stabilizes the complex over 3000-fold and prevents the basic region of Jun from binding to DNA. Gel shift assays indicate that A-Fos can inactivate the DNA binding of a Fos:Jun heterodimer in an equimolar competition. Transient transfection assays indicate that A-Fos inhibits Jun-dependent transactivation. Both the acidic extension and the Fos leucine zipper are critical for this inhibition. Expression of A-Fos in mouse fibroblasts inhibits focus formation more than colony formation, reflecting the ability of A-Fos to interfere with the AP1 biological functions in mammalian cells. This reagent is more potent than a deletion of either the Fos or Jun transactivation domain, which has been used previously as a dominant negative to AP1 activity. | lld:pubmed |
| pubmed-article:9228025 | pubmed:language | eng | lld:pubmed |
| pubmed-article:9228025 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9228025 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:9228025 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:9228025 | pubmed:month | Jul | lld:pubmed |
| pubmed-article:9228025 | pubmed:issn | 0021-9258 | lld:pubmed |
| pubmed-article:9228025 | pubmed:author | pubmed-author:OlivaAA | lld:pubmed |
| pubmed-article:9228025 | pubmed:author | pubmed-author:GardnerKK | lld:pubmed |
| pubmed-article:9228025 | pubmed:author | pubmed-author:VinsonCC | lld:pubmed |
| pubmed-article:9228025 | pubmed:author | pubmed-author:TaparowskyEE | lld:pubmed |
| pubmed-article:9228025 | pubmed:author | pubmed-author:KrylovDD | lld:pubmed |
| pubmed-article:9228025 | pubmed:author | pubmed-author:EchlinD RDR | lld:pubmed |
| pubmed-article:9228025 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:9228025 | pubmed:day | 25 | lld:pubmed |
| pubmed-article:9228025 | pubmed:volume | 272 | lld:pubmed |
| pubmed-article:9228025 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:9228025 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:9228025 | pubmed:pagination | 18586-94 | lld:pubmed |
| pubmed-article:9228025 | pubmed:dateRevised | 2008-11-21 | lld:pubmed |
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| pubmed-article:9228025 | pubmed:meshHeading | pubmed-meshheading:9228025-... | lld:pubmed |
| pubmed-article:9228025 | pubmed:year | 1997 | lld:pubmed |
| pubmed-article:9228025 | pubmed:articleTitle | A dominant negative to activation protein-1 (AP1) that abolishes DNA binding and inhibits oncogenesis. | lld:pubmed |
| pubmed-article:9228025 | pubmed:affiliation | Laboratory of Biochemistry, NCI, National Institutes of Health, Bethesda, Maryland 20892, USA. | lld:pubmed |
| pubmed-article:9228025 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:9228025 | pubmed:publicationType | Research Support, U.S. Gov't, Non-P.H.S. | lld:pubmed |
| pubmed-article:9228025 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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