| pubmed-article:10495274 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:10495274 | lifeskim:mentions | umls-concept:C1517080 | lld:lifeskim |
| pubmed-article:10495274 | lifeskim:mentions | umls-concept:C0013138 | lld:lifeskim |
| pubmed-article:10495274 | lifeskim:mentions | umls-concept:C0205453 | lld:lifeskim |
| pubmed-article:10495274 | lifeskim:mentions | umls-concept:C0441712 | lld:lifeskim |
| pubmed-article:10495274 | pubmed:issue | 1-2 | lld:pubmed |
| pubmed-article:10495274 | pubmed:dateCreated | 2000-3-16 | lld:pubmed |
| pubmed-article:10495274 | pubmed:abstractText | We have examined the roles played by the Drosophila neural RNA-binding protein Musashi (MSI) in eye development. MSI expression was observed in the nuclei of all photoreceptor cells (R1-R8). Although a msi loss-of-function mutation resulted in only weak abnormalities in photoreceptor differentiation, we found that the msi eye phenotype was significantly enhanced in a seven in absentia (sina) background. sina is known to be involved in the degradation of the Tramtrack (TTK) protein, leading to the specification of the R7 fate. We demonstrated that MSI also functions to regulate TTK expression. The sina msi mutants showed significantly high ectopic expression of TTK69 and failure in the determination of the R1, R6, and R7 fates. Other photoreceptor cells also failed to differentiate with abnormalities occurring late in the differentiation process. These results suggest that MSI and SINA function redundantly to downregulate TTK in developing photoreceptor cells. | lld:pubmed |
| pubmed-article:10495274 | pubmed:language | eng | lld:pubmed |
| pubmed-article:10495274 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10495274 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:10495274 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10495274 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:10495274 | pubmed:month | Sep | lld:pubmed |
| pubmed-article:10495274 | pubmed:issn | 0925-4773 | lld:pubmed |
| pubmed-article:10495274 | pubmed:author | pubmed-author:KurusuMM | lld:pubmed |
| pubmed-article:10495274 | pubmed:author | pubmed-author:NakamuraMM | lld:pubmed |
| pubmed-article:10495274 | pubmed:author | pubmed-author:YamamotoAA | lld:pubmed |
| pubmed-article:10495274 | pubmed:author | pubmed-author:OkabeMM | lld:pubmed |
| pubmed-article:10495274 | pubmed:author | pubmed-author:ImaiTT | lld:pubmed |
| pubmed-article:10495274 | pubmed:author | pubmed-author:HirotaYY | lld:pubmed |
| pubmed-article:10495274 | pubmed:author | pubmed-author:OkanoHH | lld:pubmed |
| pubmed-article:10495274 | pubmed:author | pubmed-author:MiyaoSS | lld:pubmed |
| pubmed-article:10495274 | pubmed:author | pubmed-author:SawamotoKK | lld:pubmed |
| pubmed-article:10495274 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:10495274 | pubmed:volume | 87 | lld:pubmed |
| pubmed-article:10495274 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:10495274 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:10495274 | pubmed:pagination | 93-101 | lld:pubmed |
| pubmed-article:10495274 | pubmed:dateRevised | 2008-11-21 | lld:pubmed |
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| pubmed-article:10495274 | pubmed:meshHeading | pubmed-meshheading:10495274... | lld:pubmed |
| pubmed-article:10495274 | pubmed:year | 1999 | lld:pubmed |
| pubmed-article:10495274 | pubmed:articleTitle | Musashi and seven in absentia downregulate Tramtrack through distinct mechanisms in Drosophila eye development. | lld:pubmed |
| pubmed-article:10495274 | pubmed:affiliation | Division of Neuroanatomy (D12), Department of Neuroscience, Biomedical Research Center, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita, Osaka, Japan. | lld:pubmed |
| pubmed-article:10495274 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:10495274 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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