Reference Report
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| Citation | Beckstead, R., Ortiz, J.A., Sanchez, C., Prokopenko, S.N., Chambon, P., Losson, R., Bellen, H.J. (2001). Bonus, a Drosophila homolog of TIF1 proteins, interacts with nuclear receptors and can inhibit FTZ-F1-dependent transcription. Mol. Cell 7(4): 753--765. (Export to RIS) | ||
| FlyBase ID | FBrf0135890 | ||
| Publication Type | Research paper | ||
| PubMed ID | 11336699 | ||
| PubMed Abstract | The Drosophila bonus (bon) gene encodes a homolog of the vertebrate TIF1 transcriptional cofactors. bon is required for male viability, molting, and numerous events in metamorphosis including leg elongation, bristle development, and pigmentation. Most of these processes are associated with genes that have been implicated in the ecdysone pathway, a nuclear hormone receptor pathway required throughout Drosophila development. Bon is associated with sites on the polytene chromosomes and can interact with numerous Drosophila nuclear receptor proteins. Bon binds via an LxxLL motif to the AF-2 activation domain present in the ligand binding domain of betaFTZ-F1 and behaves as a transcriptional inhibitor in vivo. | ||
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| Supplementary material | Supplemental data. [FBrf0137448] |
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| Language of Publication | English | ||
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Parent Publication
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| Publication Type | Journal | ||
| Abbreviation | Mol. Cell | ||
| Title | Molecular Cell | ||
| Publication Year | 1997- | ||
| ISBN/ISSN | 1097-2765 1097-4164 | ||
Data from Reference
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Aberrations (2)
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Alleles (20)
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Constructs (1)
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Genes (10)
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Insertions (3)
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