| pubmed-article:8754851 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:8754851 | lifeskim:mentions | umls-concept:C0006826 | lld:lifeskim |
| pubmed-article:8754851 | lifeskim:mentions | umls-concept:C0162508 | lld:lifeskim |
| pubmed-article:8754851 | lifeskim:mentions | umls-concept:C1510411 | lld:lifeskim |
| pubmed-article:8754851 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
| pubmed-article:8754851 | lifeskim:mentions | umls-concept:C1546857 | lld:lifeskim |
| pubmed-article:8754851 | pubmed:issue | 8 | lld:pubmed |
| pubmed-article:8754851 | pubmed:dateCreated | 1996-9-20 | lld:pubmed |
| pubmed-article:8754851 | pubmed:abstractText | ras is an important oncogene in experimental animals and humans. In addition, activated ras proteins are potent inducers of the transcription factor AP-1, which is composed of heterodimeric complexes of Fos and Jun proteins. Together with the fact that deregulated expression of some AP-1 proteins can cause neoplastic transformation, this finding suggests that AP-1 may function as a critical ras effector. We have tested this hypothesis directly by analyzing the response to activated ras in cells that harbor a null mutation in the c-jun gene. The transcriptional response of AP-1-responsive genes to activated ras is severely impaired in c-jun null fibroblasts. Compared with wild-type cells, the c-jun null cells lack many characteristics of ras transformation, including loss of contact inhibition, anchorage independence, and tumorigenicity in nude mice; these properties are restored by forced expression of c-jun. Rare tumorigenic variants of ras-expressing c-jun null fibroblasts do arise. Analysis of these variants reveals a consistent restoration of AP-1 activity. The results provide genetic evidence that c-jun is a crucial effector for transformation by activated ras proteins. | lld:pubmed |
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| pubmed-article:8754851 | pubmed:language | eng | lld:pubmed |
| pubmed-article:8754851 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8754851 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:8754851 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8754851 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8754851 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8754851 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:8754851 | pubmed:month | Aug | lld:pubmed |
| pubmed-article:8754851 | pubmed:issn | 0270-7306 | lld:pubmed |
| pubmed-article:8754851 | pubmed:author | pubmed-author:JohnsonRR | lld:pubmed |
| pubmed-article:8754851 | pubmed:author | pubmed-author:HanahanDD | lld:pubmed |
| pubmed-article:8754851 | pubmed:author | pubmed-author:WisdomRR | lld:pubmed |
| pubmed-article:8754851 | pubmed:author | pubmed-author:SpiegelmanBB | lld:pubmed |
| pubmed-article:8754851 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:8754851 | pubmed:volume | 16 | lld:pubmed |
| pubmed-article:8754851 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:8754851 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:8754851 | pubmed:pagination | 4504-11 | lld:pubmed |
| pubmed-article:8754851 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
| pubmed-article:8754851 | pubmed:meshHeading | pubmed-meshheading:8754851-... | lld:pubmed |
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| pubmed-article:8754851 | pubmed:meshHeading | pubmed-meshheading:8754851-... | lld:pubmed |
| pubmed-article:8754851 | pubmed:meshHeading | pubmed-meshheading:8754851-... | lld:pubmed |
| pubmed-article:8754851 | pubmed:meshHeading | pubmed-meshheading:8754851-... | lld:pubmed |
| pubmed-article:8754851 | pubmed:year | 1996 | lld:pubmed |
| pubmed-article:8754851 | pubmed:articleTitle | Cellular transformation and malignancy induced by ras require c-jun. | lld:pubmed |
| pubmed-article:8754851 | pubmed:affiliation | Hormone Research Institute, University of California, San Francisco 94143, USA. | lld:pubmed |
