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Science 18 May 1990: Vol. 248. no. 4957, pp. 857 - 860 DOI: 10.1126/science.2188361
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Articles
Science, Vol 248, Issue 4957, 857-860
Copyright © 1990 by American Association for the Advancement of Science
Genetic suppression of mutations in the Drosophila abl proto-oncogene homolog
FB Gertler,
JS Doctor,
and
FM Hoffmann
McArdle Laboratory for Cancer Research, University of Wisconsin, Madison 53706.
The Drosophila abelson (abl) gene encodes the homolog of the mammalian c-abl cytoplasmic tyrosine kinase and is an essential gene for the development of viable adult flies. Three second-site mutations that suppress the lethality caused by the absence of abl function have been isolated, and all three map to the gene enabled (ena). The mutations are recessive embryonic lethal mutations but act as dominant mutations to compensate for the neural defects of abl mutants. Thus, mutations in a specific gene can compensate for the absence of a tyrosine kinase.
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- enabled, a dosage-sensitive suppressor of mutations in the Drosophila Abl tyrosine kinase, encodes an Abl substrate with SH3 domain-binding properties..
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Genes & Dev.
9, 521-533
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- Dosage-sensitive modifiers of Drosophila abl tyrosine kinase function: prospero, a regulator of axonal outgrowth, and disabled, a novel tyrosine kinase substrate..
- F B Gertler, K K Hill, M J Clark, and F M Hoffmann (1993)
Genes & Dev.
7, 441-453
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- Increased levels of the Drosophila Abelson tyrosine kinase in nerves and muscles: subcellular localization and mutant phenotypes imply a role in cell-cell interactions.
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| Abstract »
| Full Text »
| PDF »
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