| pubmed-article:12079506 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:12079506 | lifeskim:mentions | umls-concept:C0521451 | lld:lifeskim |
| pubmed-article:12079506 | lifeskim:mentions | umls-concept:C0139030 | lld:lifeskim |
| pubmed-article:12079506 | lifeskim:mentions | umls-concept:C0205160 | lld:lifeskim |
| pubmed-article:12079506 | lifeskim:mentions | umls-concept:C1710595 | lld:lifeskim |
| pubmed-article:12079506 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
| pubmed-article:12079506 | lifeskim:mentions | umls-concept:C0439799 | lld:lifeskim |
| pubmed-article:12079506 | pubmed:dateCreated | 2002-6-24 | lld:pubmed |
| pubmed-article:12079506 | pubmed:abstractText | Growth of cancer cells results from the disturbance of positive and negative growth control mechanisms and the prolonged survival of these genetically altered cells due to the failure of cellular suicide programs. Genetic and biochemical approaches have identified Raf family serine/threonine kinases B-Raf and C-Raf as major mediators of cell survival. C-Raf cooperates with Bcl-2/Bcl-XL in suppression of apoptosis by a mechanism that involves targeting of C-Raf to the outer mitochondrial membrane and inactivation of the pro-apoptotic protein Bad. However, apoptosis suppression by C-Raf also occurs in cells lacking expression of Bad or Bcl-2. | lld:pubmed |
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| pubmed-article:12079506 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:12079506 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:12079506 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:12079506 | pubmed:month | Jun | lld:pubmed |
| pubmed-article:12079506 | pubmed:issn | 1471-2121 | lld:pubmed |
| pubmed-article:12079506 | pubmed:author | pubmed-author:TroppmairJako... | lld:pubmed |
| pubmed-article:12079506 | pubmed:author | pubmed-author:BenzRolandR | lld:pubmed |
| pubmed-article:12079506 | pubmed:author | pubmed-author:RappUlf RUR | lld:pubmed |
| pubmed-article:12079506 | pubmed:author | pubmed-author:Le... | lld:pubmed |
| pubmed-article:12079506 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:12079506 | pubmed:day | 12 | lld:pubmed |
| pubmed-article:12079506 | pubmed:volume | 3 | lld:pubmed |
| pubmed-article:12079506 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:12079506 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:12079506 | pubmed:pagination | 14 | lld:pubmed |
| pubmed-article:12079506 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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| pubmed-article:12079506 | pubmed:year | 2002 | lld:pubmed |
| pubmed-article:12079506 | pubmed:articleTitle | Negative regulation of mitochondrial VDAC channels by C-Raf kinase. | lld:pubmed |
| pubmed-article:12079506 | pubmed:affiliation | Institut für Medizinische Strahlenkunde und Zellforschung (MSZ), Universität Würzburg, 97078 Würzburg, Germany. lemellay@univ-montp2.fr | lld:pubmed |
| pubmed-article:12079506 | pubmed:publicationType | Journal Article | lld:pubmed |
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