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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.

Gertler, F B, Hill, K K, Clark, M J, Hoffmann, F M·1993·Genes & Development

Abstract

In the absence of the Drosophila abl protein-tyrosine kinase (PTK), loss-of-function mutations in either disabled or prospero have dominant phenotypic effects on embryonic development. Molecular and genetic characterizations indicate that the products of these genes interact with the abl PTK by different mechanisms. The interaction between abl and prospero, which encodes a nuclear protein required for correct axonal outgrowth, is likely to be indirect. In contrast, the product of disabled may be a substrate for the abl PTK. The disabled protein is colocalized with abl in axons, its predicted amino acid sequence contains 10 motifs similar to the major autophosphorylation site of abl, and the protein is recognized by antibodies to phosphotyrosine.

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  • Dab2 is one of two mammalian orthologs of the Drosophila Disabled (dDab), a family member of the Disabled proteins involved in neurogenesis, oncogenesis, cellular signaling and embryonic development.

    “Subsequent studies indicated Dab2 as one of two mammalian orthologs of the Drosophila Disabled (dDab) [8-11], a family member of the Disabled proteins involved in neurogenesis, oncogenesis, cellular signaling and embryonic development.”

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Metadata

Authors
Gertler, F. B., Hill, K. K., Clark, M. J., & Hoffmann, F. M.
Venue
Genes & Development
Published
1993-03
Volume
7
Issue
3
Pages
441-453
ISSN
  • 0890-9369
  • 1549-5477
Cited by
111
References
1
Language
en

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