| pubmed-article:15254235 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:15254235 | lifeskim:mentions | umls-concept:C0138965 | lld:lifeskim |
| pubmed-article:15254235 | lifeskim:mentions | umls-concept:C1335960 | lld:lifeskim |
| pubmed-article:15254235 | lifeskim:mentions | umls-concept:C0596290 | lld:lifeskim |
| pubmed-article:15254235 | lifeskim:mentions | umls-concept:C0021467 | lld:lifeskim |
| pubmed-article:15254235 | lifeskim:mentions | umls-concept:C0805732 | lld:lifeskim |
| pubmed-article:15254235 | lifeskim:mentions | umls-concept:C1366753 | lld:lifeskim |
| pubmed-article:15254235 | lifeskim:mentions | umls-concept:C1367731 | lld:lifeskim |
| pubmed-article:15254235 | lifeskim:mentions | umls-concept:C0013138 | lld:lifeskim |
| pubmed-article:15254235 | lifeskim:mentions | umls-concept:C1523713 | lld:lifeskim |
| pubmed-article:15254235 | lifeskim:mentions | umls-concept:C1704259 | lld:lifeskim |
| pubmed-article:15254235 | lifeskim:mentions | umls-concept:C0021469 | lld:lifeskim |
| pubmed-article:15254235 | lifeskim:mentions | umls-concept:C1705987 | lld:lifeskim |
| pubmed-article:15254235 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
| pubmed-article:15254235 | lifeskim:mentions | umls-concept:C0205548 | lld:lifeskim |
| pubmed-article:15254235 | lifeskim:mentions | umls-concept:C1548425 | lld:lifeskim |
| pubmed-article:15254235 | pubmed:issue | 15 | lld:pubmed |
| pubmed-article:15254235 | pubmed:dateCreated | 2004-7-15 | lld:pubmed |
| pubmed-article:15254235 | pubmed:abstractText | Src family kinases regulate multiple cellular processes including proliferation and oncogenesis. C-terminal Src kinase (Csk) encodes a critical negative regulator of Src family kinases. We demonstrate that the Drosophila melanogaster Csk ortholog, dCsk, functions as a tumor suppressor: dCsk mutants display organ overgrowth and excess cellular proliferation. Genetic analysis indicates that the dCsk(-/-) overgrowth phenotype results from activation of Src, Jun kinase, and STAT signal transduction pathways. In particular, blockade of STAT function in dCsk mutants severely reduced Src-dependent overgrowth and activated apoptosis of mutant tissue. Our data provide in vivo evidence that Src activity requires JNK and STAT function. | lld:pubmed |
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| pubmed-article:15254235 | pubmed:language | eng | lld:pubmed |
| pubmed-article:15254235 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15254235 | pubmed:citationSubset | IM | lld:pubmed |
