| pubmed-article:8816487 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:8816487 | lifeskim:mentions | umls-concept:C0001483 | lld:lifeskim |
| pubmed-article:8816487 | lifeskim:mentions | umls-concept:C1709313 | lld:lifeskim |
| pubmed-article:8816487 | lifeskim:mentions | umls-concept:C0162493 | lld:lifeskim |
| pubmed-article:8816487 | lifeskim:mentions | umls-concept:C1335840 | lld:lifeskim |
| pubmed-article:8816487 | lifeskim:mentions | umls-concept:C1533157 | lld:lifeskim |
| pubmed-article:8816487 | pubmed:issue | 10 | lld:pubmed |
| pubmed-article:8816487 | pubmed:dateCreated | 1996-11-15 | lld:pubmed |
| pubmed-article:8816487 | pubmed:abstractText | Expression of the adenovirus E1A243 oncoprotein in Saccharomyces cerevisiae produces a slow-growth phenotype with accumulation of cells in the G1 phase of the cell cycle. This effect is due to the N-terminal and CR1 domains of E1A243, which in rodent cells are involved in triggering cellular transformation and also in binding to the cellular transcriptional coactivator p300. A genetic screen was undertaken to identify genes required for the function of E1A243 in S. cerevisiae. This screen identified SNF12, a gene encoding the 73-kDa subunit of the SWI/SNF transcriptional regulatory complex. Mutation of genes encoding known members of the SWI/SNF complex also led to loss of E1A function, suggesting that the SWI/SNF complex is a target of E1A243. Moreover, expression of E1A in wild-type cells specifically blocked transcriptional activation of the INO1 and SUC2 genes, whose activation pathways are distinct but have a common requirement for the SWI/SNF complex. These data demonstrate a specific functional interaction between E1A and the SWI/SNF complex and suggest that a similar interaction takes place in rodent and human cells. | lld:pubmed |
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| pubmed-article:8816487 | pubmed:language | eng | lld:pubmed |
| pubmed-article:8816487 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8816487 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:8816487 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:8816487 | pubmed:month | Oct | lld:pubmed |
| pubmed-article:8816487 | pubmed:issn | 0270-7306 | lld:pubmed |
| pubmed-article:8816487 | pubmed:author | pubmed-author:MillerM EME | lld:pubmed |
| pubmed-article:8816487 | pubmed:author | pubmed-author:LevinsonR SRS | lld:pubmed |
| pubmed-article:8816487 | pubmed:author | pubmed-author:SmithM MMM | lld:pubmed |
| pubmed-article:8816487 | pubmed:author | pubmed-author:YamamotoK RKR | lld:pubmed |
| pubmed-article:8816487 | pubmed:author | pubmed-author:EngelD ADA | lld:pubmed |
| pubmed-article:8816487 | pubmed:author | pubmed-author:CairnsB RBR | lld:pubmed |
| pubmed-article:8816487 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:8816487 | pubmed:volume | 16 | lld:pubmed |
| pubmed-article:8816487 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:8816487 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:8816487 | pubmed:pagination | 5737-43 | lld:pubmed |
| pubmed-article:8816487 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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