| pubmed-article:12183376 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:12183376 | lifeskim:mentions | umls-concept:C1335960 | lld:lifeskim |
| pubmed-article:12183376 | lifeskim:mentions | umls-concept:C0460005 | lld:lifeskim |
| pubmed-article:12183376 | lifeskim:mentions | umls-concept:C0206364 | lld:lifeskim |
| pubmed-article:12183376 | lifeskim:mentions | umls-concept:C0805732 | lld:lifeskim |
| pubmed-article:12183376 | lifeskim:mentions | umls-concept:C1366753 | lld:lifeskim |
| pubmed-article:12183376 | lifeskim:mentions | umls-concept:C0013138 | lld:lifeskim |
| pubmed-article:12183376 | lifeskim:mentions | umls-concept:C0443199 | lld:lifeskim |
| pubmed-article:12183376 | lifeskim:mentions | umls-concept:C0205548 | lld:lifeskim |
| pubmed-article:12183376 | lifeskim:mentions | umls-concept:C1548425 | lld:lifeskim |
| pubmed-article:12183376 | lifeskim:mentions | umls-concept:C1514873 | lld:lifeskim |
| pubmed-article:12183376 | pubmed:issue | 18 | lld:pubmed |
| pubmed-article:12183376 | pubmed:dateCreated | 2002-8-16 | lld:pubmed |
| pubmed-article:12183376 | pubmed:abstractText | Malignant transformation frequently involves aberrant signaling from receptor tyrosine kinases (RTKs). These receptors commonly activate Ras/Raf/MEK/MAPK signaling but when overactivated can also induce the JAK/STAT pathway, originally identified as the signaling cascade downstream of cytokine receptors. Inappropriate activation of STAT has been found in many human cancers. However, the contribution of the JAK/STAT pathway in RTK signaling remains unclear. We have investigated the requirement of the JAK/STAT pathway for signaling by wild-type and mutant forms of the RTK Torso (Tor) using a genetic approach in Drosophila. Our results indicate that the JAK/STAT pathway plays little or no role in signaling by wild-type Tor. In contrast, we find that STAT, encoded by marelle (mrl; DStat92E), is essential for the gain-of-function mutant Tor (Tor(GOF)) to activate ectopic gene expression. Our findings indicate that the Ras/Raf/MEK/MAPK signaling pathway is sufficient to mediate the normal functions of wild-type RTK, whereas the effects of gain-of-function mutant RTK additionally require STAT activation. | lld:pubmed |
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| pubmed-article:12183376 | pubmed:language | eng | lld:pubmed |
| pubmed-article:12183376 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12183376 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:12183376 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:12183376 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:12183376 | pubmed:month | Sep | lld:pubmed |
| pubmed-article:12183376 | pubmed:issn | 0950-1991 | lld:pubmed |
| pubmed-article:12183376 | pubmed:author | pubmed-author:PerrimonNorbe... | lld:pubmed |
| pubmed-article:12183376 | pubmed:author | pubmed-author:Mathey-Prevot... | lld:pubmed |
| pubmed-article:12183376 | pubmed:author | pubmed-author:LiWillis XWX | lld:pubmed |
| pubmed-article:12183376 | pubmed:author | pubmed-author:AgaisseHerveH | lld:pubmed |
| pubmed-article:12183376 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:12183376 | pubmed:volume | 129 | lld:pubmed |
| pubmed-article:12183376 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:12183376 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:12183376 | pubmed:pagination | 4241-8 | lld:pubmed |
| pubmed-article:12183376 | pubmed:dateRevised | 2011-7-28 | lld:pubmed |
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| pubmed-article:12183376 | pubmed:meshHeading | pubmed-meshheading:12183376... | lld:pubmed |
| pubmed-article:12183376 | pubmed:meshHeading | pubmed-meshheading:12183376... | lld:pubmed |
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| pubmed-article:12183376 | pubmed:meshHeading | pubmed-meshheading:12183376... | lld:pubmed |
| pubmed-article:12183376 | pubmed:meshHeading | pubmed-meshheading:12183376... | lld:pubmed |
| pubmed-article:12183376 | pubmed:meshHeading | pubmed-meshheading:12183376... | lld:pubmed |
| pubmed-article:12183376 | pubmed:meshHeading | pubmed-meshheading:12183376... | lld:pubmed |
| pubmed-article:12183376 | pubmed:meshHeading | pubmed-meshheading:12183376... | lld:pubmed |
| pubmed-article:12183376 | pubmed:meshHeading | pubmed-meshheading:12183376... | lld:pubmed |
| pubmed-article:12183376 | pubmed:meshHeading | pubmed-meshheading:12183376... | lld:pubmed |
| pubmed-article:12183376 | pubmed:meshHeading | pubmed-meshheading:12183376... | lld:pubmed |
| pubmed-article:12183376 | pubmed:meshHeading | pubmed-meshheading:12183376... | lld:pubmed |
| pubmed-article:12183376 | pubmed:year | 2002 | lld:pubmed |
| pubmed-article:12183376 | pubmed:articleTitle | Differential requirement for STAT by gain-of-function and wild-type receptor tyrosine kinase Torso in Drosophila. | lld:pubmed |
| pubmed-article:12183376 | pubmed:affiliation | Department of Genetics, Harvard Medical School, 200 Longwood Avenue, Boston, MA 02115, USA. willis_li@URMC.Rochester.edu | lld:pubmed |
| pubmed-article:12183376 | pubmed:publicationType | Journal Article | lld:pubmed |
