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Differential interaction and activation of Rho family GTPases by p210bcr-abl and p190bcr-abl

Harnois, Thomas, Constantin, Bruno, Rioux, Agnès, Grenioux, Eddy, Kitzis, Alain, Bourmeyster, Nicolas·2003·Oncogene
DOI 10.1038/sj.onc.1206626
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Abstract

The p210(bcr-abl) and p190(bcr-abl) fusion proteins, respectively responsible for chronic myelogenous leukemia and acute lymphoblastic leukemia, present deregulated tyrosine kinase activity and abnormal localization. The Dbl homology domain of Bcr, activating Rho GTPases, is present in p210(bcr-abl), but absent in p190(bcr-abl). We investigated the interaction of Bcr-Abl chimeras and Rho proteins by coimmunoprecipitation, pull-down experiments and GEF activity measurement. RhoA, Rac1 and Cdc42 interact in vivo with p210(bcr-abl) only. Moreover, the three types of GTPases are activated in vitro and in vivo by p210(bcr-abl). Nevertheless, Rac1 and Cdc42, but not RhoA, are activated by p190(bcr-abl) in vitro and in vivo. Part of this GEF activity of p190(bcr-abl) is probably attributable to p95(vav), which is complexed with both p190(bcr-abl) and p210(bcr-abl) in an activated form. p160(bcr), also in complex with Bcr-Abl, presents no GEF activity in p190(bcr-abl)-expressing cells. These results suggest that differential activation of Rho proteins should play a major role in Bcr-Abl-induced leukemogenesis.

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Metadata

Authors
Harnois, T., Constantin, B., Rioux, A., Grenioux, E., Kitzis, A., & Bourmeyster, N.
Venue
Oncogene
Publisher
Springer Science and Business Media LLC
Published
2003-09-25
Volume
22
Issue
41
Pages
6445-6454
ISSN
  • 0950-9232
  • 1476-5594
DOI
10.1038/sj.onc.1206626
Cited by
58
References
1
Language
en
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CoChat. (2026). Citation check: Differential interaction and activation of Rho family GTPases by p210bcr-abl and p190bcr-abl. https://app.cochat.ai/papers/10.1038/sj.onc.1206626
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Harnois, T., Constantin, B., Rioux, A., Grenioux, E., Kitzis, A., & Bourmeyster, N. (2003). Differential interaction and activation of Rho family GTPases by p210bcr-abl and p190bcr-abl. Oncogene. https://doi.org/10.1038/sj.onc.1206626