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Gene Review

Abi1  -  abl-interactor 1

Mus musculus

Synonyms: Abelson interactor 1, Abi-1, Abl interactor 1, Ablphilin-1, E3B1, ...
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High impact information on Abi1

  • We suggest that the Abi-1 protein may serve as a regulator of Abl function in transformation or in signal transduction [1].
  • A novel cellular protein, Abl-interactor-1 (Abi-1), which specifically interacts with the carboxy-terminal region of Abl oncoproteins, has been identified in a mouse leukemia cell line [1].
  • Conversely, full-length Eps8 is auto-inhibited in vitro, and interaction with the Abi1 protein relieves this inhibition [2].
  • Sra-1 and Nap1 link Rac to actin assembly driving lamellipodia formation [3].
  • Thus, Abi-1 undergoes nucleocytoplasmic shuttling and functions at the leading edge to regulate Wave-1 localization and protein levels [4].

Biological context of Abi1


Anatomical context of Abi1

  • Altogether these data identify a WAVE2-Abi1 complex crucial for the normal actin cytoskeleton reorganization and migration of macrophages in response to CSF-1 [5].
  • Inhibition of v-Abl transformation in 3T3 cells overexpressing different forms of the Abelson interactor protein Abi-1 [7].
  • The axis duplications arise because Nap1 is required for the normal polarization and migration of cells of the Anterior Visceral Endoderm (AVE), an early extraembryonic organizer tissue [6].
  • Other morphogenetic processes appear to proceed normally in the absence of Nap1/WAVE activity: the notochord, the layers of the heart, and the epithelial-to-mesenchymal transition (EMT) at gastrulation appear normal [6].
  • Here, we show that mouse embryos that lack Nap1, a regulatory component of the WAVE complex, arrest at midgestation and have defects in morphogenesis of all three embryonic germ layers [6].

Associations of Abi1 with chemical compounds

  • Further, we demonstrated that Abi-1 shuttles in and out of the nucleus in a leptomycin B (LMB)-dependent manner and that complete nuclear translocation of Abi-1 in the absence of LMB requires the combined inactivation of the SNARE, WAB, and SH3 domains of Abi-1 [4].

Physical interactions of Abi1

  • WAVE2 was found in a protein complex together with Abelson kinase interactor 1 (Abi1) in resting or stimulated cells [5].

Other interactions of Abi1

  • Both WAVE2 and Abi1 were recruited to and necessary for the formation of F-actin protrusions in response to CSF-1 [5].


  1. Abl-interactor-1, a novel SH3 protein binding to the carboxy-terminal portion of the Abl protein, suppresses v-abl transforming activity. Shi, Y., Alin, K., Goff, S.P. Genes Dev. (1995) [Pubmed]
  2. Eps8 controls actin-based motility by capping the barbed ends of actin filaments. Disanza, A., Carlier, M.F., Stradal, T.E., Didry, D., Frittoli, E., Confalonieri, S., Croce, A., Wehland, J., Di Fiore, P.P., Scita, G. Nat. Cell Biol. (2004) [Pubmed]
  3. Sra-1 and Nap1 link Rac to actin assembly driving lamellipodia formation. Steffen, A., Rottner, K., Ehinger, J., Innocenti, M., Scita, G., Wehland, J., Stradal, T.E. EMBO J. (2004) [Pubmed]
  4. Abl interactor 1 (Abi-1) wave-binding and SNARE domains regulate its nucleocytoplasmic shuttling, lamellipodium localization, and wave-1 levels. Echarri, A., Lai, M.J., Robinson, M.R., Pendergast, A.M. Mol. Cell. Biol. (2004) [Pubmed]
  5. A WAVE2-Abi1 complex mediates CSF-1-induced F-actin-rich membrane protrusions and migration in macrophages. Kheir, W.A., Gevrey, J.C., Yamaguchi, H., Isaac, B., Cox, D. J. Cell. Sci. (2005) [Pubmed]
  6. Axis specification and morphogenesis in the mouse embryo require Nap1, a regulator of WAVE-mediated actin branching. Rakeman, A.S., Anderson, K.V. Development (2006) [Pubmed]
  7. Inhibition of v-Abl transformation in 3T3 cells overexpressing different forms of the Abelson interactor protein Abi-1. Ikeguchi, A., Yang, H.Y., Gao, G., Goff, S.P. Oncogene (2001) [Pubmed]
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