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Gene Review

Dab  -  Disabled

Drosophila melanogaster

Synonyms: CG9695, Dmel\CG9695, Protein disabled, cDNA C, dab
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High impact information on Dab

  • Embryos that are homozygous mutant for both abl and dab fail to develop any axon bundles in the CNS, although the peripheral nervous system and the larval cuticle appear normal [1].
  • Here, we identify a mouse homolog of the Drosophila Disabled (Dab) protein, mDab1, and show it is an adaptor molecule functioning in neural development [2].
  • The properties of mDab1 and genetic analysis of Dab in Drosophila suggest that these molecules function in key signal transduction pathways involved in the formation of neural networks [2].
  • We show that the phosphotyrosine-binding (PTB) domain-containing protein Disabled (DAB) binds to the DRK SH3 domains [3].
  • These findings suggest that simultaneous interaction of the rigid DH domain with the NPXY sequence and PtdIns-4,5-P2 plays a role in the attachment of Dab proteins to the APP/lipoprotein receptors and phosphoinositide-rich membranes [4].

Other interactions of Dab

  • Two prominent genes that arose from these screens were enabled (Ena) and disabled (Dab) [5].


  1. Drosophila abl tyrosine kinase in embryonic CNS axons: a role in axonogenesis is revealed through dosage-sensitive interactions with disabled. Gertler, F.B., Bennett, R.L., Clark, M.J., Hoffmann, F.M. Cell (1989) [Pubmed]
  2. Mouse disabled (mDab1): a Src binding protein implicated in neuronal development. Howell, B.W., Gertler, F.B., Cooper, J.A. EMBO J. (1997) [Pubmed]
  3. Disabled is a putative adaptor protein that functions during signaling by the sevenless receptor tyrosine kinase. Le, N., Simon, M.A. Mol. Cell. Biol. (1998) [Pubmed]
  4. Crystal structures of the Dab homology domains of mouse disabled 1 and 2. Yun, M., Keshvara, L., Park, C.G., Zhang, Y.M., Dickerson, J.B., Zheng, J., Rock, C.O., Curran, T., Park, H.W. J. Biol. Chem. (2003) [Pubmed]
  5. Filopodia formation and Disabled degradation downstream of Reelin. Winder, S.J. Biochem. J. (2004) [Pubmed]
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