pubmed-article:9926937 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:9926937 | lifeskim:mentions | umls-concept:C0029016 | lld:lifeskim |
pubmed-article:9926937 | lifeskim:mentions | umls-concept:C1280500 | lld:lifeskim |
pubmed-article:9926937 | lifeskim:mentions | umls-concept:C0026559 | lld:lifeskim |
pubmed-article:9926937 | lifeskim:mentions | umls-concept:C0013138 | lld:lifeskim |
pubmed-article:9926937 | lifeskim:mentions | umls-concept:C1527180 | lld:lifeskim |
pubmed-article:9926937 | pubmed:issue | 1 | lld:pubmed |
pubmed-article:9926937 | pubmed:dateCreated | 1999-2-26 | lld:pubmed |
pubmed-article:9926937 | pubmed:abstractText | We targeted expression of human/fly chimeric Bcr-Abl proteins to the developing central nervous system (CNS) and eye imaginal disc of Drosophila melanogaster. Neural expression of human/fly chimeric P210 Bcr-Abl or P185 Bcr-Abl rescued abl mutant flies from pupal lethality, indicating that P210 and P185 Bcr-Abl can substitute functionally for Drosophila Abl during axonogenesis. However, increased levels of neurally expressed P210 or P185 Bcr-Abl but not Drosophila Abl produced CNS defects and lethality. Expression of P210 or P185 in the eye imaginal disc produced a dominant rough eye phenotype that was dependent on dosage of the transgene. Drosophila Enabled, previously identified as a suppressor of the abl mutant phenotype and substrate for Drosophila Abl kinase, had markedly increased phosphotyrosine levels in Bcr-Abl expressing Drosophila, indicating that it is a substrate for Bcr-Abl as well. Drosophila, therefore, is a suitable model system to identify Bcr-Abl interactions important for signal transduction and oncogenesis. | lld:pubmed |
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pubmed-article:9926937 | pubmed:language | eng | lld:pubmed |
pubmed-article:9926937 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9926937 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:9926937 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:9926937 | pubmed:month | Jan | lld:pubmed |
pubmed-article:9926937 | pubmed:issn | 0950-9232 | lld:pubmed |
pubmed-article:9926937 | pubmed:author | pubmed-author:HoffmannF MFM | lld:pubmed |
pubmed-article:9926937 | pubmed:author | pubmed-author:PetersenJJ | lld:pubmed |
pubmed-article:9926937 | pubmed:author | pubmed-author:MosherD FDF | lld:pubmed |
pubmed-article:9926937 | pubmed:author | pubmed-author:ClarkM JMJ | lld:pubmed |
pubmed-article:9926937 | pubmed:author | pubmed-author:JuangJ LJL | lld:pubmed |
pubmed-article:9926937 | pubmed:author | pubmed-author:FogertyF JFJ | lld:pubmed |
pubmed-article:9926937 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:9926937 | pubmed:day | 7 | lld:pubmed |
pubmed-article:9926937 | pubmed:volume | 18 | lld:pubmed |
pubmed-article:9926937 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:9926937 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:9926937 | pubmed:pagination | 219-32 | lld:pubmed |
pubmed-article:9926937 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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pubmed-article:9926937 | pubmed:year | 1999 | lld:pubmed |
pubmed-article:9926937 | pubmed:articleTitle | Dominant effects of the bcr-abl oncogene on Drosophila morphogenesis. | lld:pubmed |
pubmed-article:9926937 | pubmed:affiliation | Department of Medicine, University of Wisconsin Comprehensive Cancer Center, Madison 53706, USA. | lld:pubmed |
pubmed-article:9926937 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:9926937 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
pubmed-article:9926937 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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