pubmed-article:10504052 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:10504052 | lifeskim:mentions | umls-concept:C0086418 | lld:lifeskim |
pubmed-article:10504052 | lifeskim:mentions | umls-concept:C0025202 | lld:lifeskim |
pubmed-article:10504052 | lifeskim:mentions | umls-concept:C0085112 | lld:lifeskim |
pubmed-article:10504052 | lifeskim:mentions | umls-concept:C0026882 | lld:lifeskim |
pubmed-article:10504052 | lifeskim:mentions | umls-concept:C0376515 | lld:lifeskim |
pubmed-article:10504052 | lifeskim:mentions | umls-concept:C1533691 | lld:lifeskim |
pubmed-article:10504052 | pubmed:issue | 4 | lld:pubmed |
pubmed-article:10504052 | pubmed:dateCreated | 1999-11-18 | lld:pubmed |
pubmed-article:10504052 | pubmed:abstractText | Activation of the N-ras gene by point mutation occurs in about 15% of all human melanomas. In recently established severe combined immunodeficiency (SCID) mouse xenotransplantation models for human melanoma, we demonstrated that mutated N-ras not only contributes to tumour growth by enhancing cellular proliferation, but also by blocking apoptosis. Mutated N-ras overexpression protected human melanomas from naturally occurring apoptosis and, in a more pronounced way, from chemotherapy-induced apoptosis in vitro and in vivo. Given the potential clinical importance of these findings we sought to determine the underlying mechanism. We found that mutated N-ras specifically upregulates the expression of the anti-apoptosis gene bcl-2 in two human melanoma cell lines in vitro and in SCID mice. Neither the expression of the anti-apoptotic protein Bcl-xL nor that of the pro-apoptotic proteins Bax and Bak were altered in cells expressing mutated N-Ras. The increase in Bcl-2 expression mediated by mutated ras therefore qualifies as a rational explanation for the enhanced chemoresistance of human melanoma expressing mutated N-Ras. | lld:pubmed |
pubmed-article:10504052 | pubmed:commentsCorrections | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10504052 | pubmed:language | eng | lld:pubmed |
pubmed-article:10504052 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10504052 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:10504052 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:10504052 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10504052 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10504052 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10504052 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10504052 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:10504052 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:10504052 | pubmed:month | Aug | lld:pubmed |
pubmed-article:10504052 | pubmed:issn | 0960-8931 | lld:pubmed |
pubmed-article:10504052 | pubmed:author | pubmed-author:PolterauerPP | lld:pubmed |
pubmed-article:10504052 | pubmed:author | pubmed-author:JansenBB | lld:pubmed |
pubmed-article:10504052 | pubmed:author | pubmed-author:SelzerEE | lld:pubmed |
pubmed-article:10504052 | pubmed:author | pubmed-author:BornerCC | lld:pubmed |
pubmed-article:10504052 | pubmed:author | pubmed-author:FellayII | lld:pubmed |
pubmed-article:10504052 | pubmed:author | pubmed-author:Schlagbauer... | lld:pubmed |
pubmed-article:10504052 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:10504052 | pubmed:volume | 9 | lld:pubmed |
pubmed-article:10504052 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:10504052 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:10504052 | pubmed:pagination | 347-50 | lld:pubmed |
pubmed-article:10504052 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
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pubmed-article:10504052 | pubmed:year | 1999 | lld:pubmed |
pubmed-article:10504052 | pubmed:articleTitle | Mutated N-ras upregulates Bcl-2 in human melanoma in vitro and in SCID mice. | lld:pubmed |
pubmed-article:10504052 | pubmed:affiliation | Institute of Biochemistry, University of Fribourg, Switzerland. | lld:pubmed |
pubmed-article:10504052 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:10504052 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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