| pubmed-article:7937838 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:7937838 | lifeskim:mentions | umls-concept:C0032556 | lld:lifeskim |
| pubmed-article:7937838 | lifeskim:mentions | umls-concept:C0162508 | lld:lifeskim |
| pubmed-article:7937838 | lifeskim:mentions | umls-concept:C0031715 | lld:lifeskim |
| pubmed-article:7937838 | lifeskim:mentions | umls-concept:C0441655 | lld:lifeskim |
| pubmed-article:7937838 | lifeskim:mentions | umls-concept:C0041361 | lld:lifeskim |
| pubmed-article:7937838 | lifeskim:mentions | umls-concept:C0040649 | lld:lifeskim |
| pubmed-article:7937838 | pubmed:issue | 21 | lld:pubmed |
| pubmed-article:7937838 | pubmed:dateCreated | 1994-11-10 | lld:pubmed |
| pubmed-article:7937838 | pubmed:abstractText | Polyomavirus middle-sized tumor antigen (MT) increases the expression of c-jun through a phorbol 12-O-tetradecanoate 13-acetate response element in the c-jun promoter. To investigate the cellular signaling pathways affected by MT, we studied the role of the c-Ras and Raf-1 proteins in MT-induced transactivation of c-jun and cell transformation. There was an increase in GTP complexed to Ras in MT-expressing cells, indicating an increase in Ras activity. Coexpression of dominant inhibitory mutants of Ha-ras and raf-1 with MT inhibited MT-mediated transactivation and focus formation. Studies of the phosphorylation of c-Jun showed that MT expression increased the phosphorylation of Ser-63 and Ser-73 in the transactivation domain and decreased the phosphorylation of a peptide containing Ser-243, Ser-249, and Thr-231 in the DNA binding domain. MT increased the transcriptional activating ability of c-Jun but failed to increase the transcriptional activating ability of c-Jun mutants with Ser-63 and Ser-73 changed to nonphosphorylatable Ala, indicating that MT modulates c-Jun activity through phosphorylation. The dominant inhibitory mutants of Ha-ras and raf-1 interfered with the ability of MT to activate c-Jun. The results indicate that MT induces a phosphorylation cascade through the activation of c-Ras and Raf-1 and that c-Jun is one of the downstream targets that may cause changes in gene expression leading to cell transformation. | lld:pubmed |
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| pubmed-article:7937838 | pubmed:language | eng | lld:pubmed |
| pubmed-article:7937838 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:7937838 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:7937838 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:7937838 | pubmed:month | Oct | lld:pubmed |
| pubmed-article:7937838 | pubmed:issn | 0027-8424 | lld:pubmed |
| pubmed-article:7937838 | pubmed:author | pubmed-author:EckhartWW | lld:pubmed |
| pubmed-article:7937838 | pubmed:author | pubmed-author:SchönthalAA | lld:pubmed |
| pubmed-article:7937838 | pubmed:author | pubmed-author:SrinivasSS | lld:pubmed |
| pubmed-article:7937838 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:7937838 | pubmed:day | 11 | lld:pubmed |
| pubmed-article:7937838 | pubmed:volume | 91 | lld:pubmed |
| pubmed-article:7937838 | pubmed:geneSymbol | c-jun | lld:pubmed |
| pubmed-article:7937838 | pubmed:geneSymbol | Ha-ras | lld:pubmed |
| pubmed-article:7937838 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:7937838 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:7937838 | pubmed:pagination | 10064-8 | lld:pubmed |
| pubmed-article:7937838 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
| pubmed-article:7937838 | pubmed:meshHeading | pubmed-meshheading:7937838-... | lld:pubmed |
| pubmed-article:7937838 | pubmed:meshHeading | pubmed-meshheading:7937838-... | lld:pubmed |
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| pubmed-article:7937838 | pubmed:meshHeading | pubmed-meshheading:7937838-... | lld:pubmed |
