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. Author manuscript; available in PMC: 2015 Jun 13.
Published in final edited form as: Leukemia. 2008 Mar 20;22(5):898–904. doi: 10.1038/leu.2008.71

Figure 1.

Figure 1

Model of activation of Rac GTPases in BCR-ABL-induced leukemogenesis. The various pathways of activation downstream of p210-BCR-ABL are indicated with different color codes. Gray-shaded areas indicate molecules or domains with guanine nucleotide exchange factor (GEF) activity. The Dbl and pleckstrin homology (Dbl and PH) domains, only present in p210-BCR-ABL, activate Rho GTPases directly. The SH3 domain in both p190- and p210-BCR-ABL activates p95Vav (Vav1). Y177/Y412, tyrosine residues that can be phosphorylated; Dbl, Rac GTPase exchange factor; SH2/SH3, Src homology domains; DD; dimerization domain; DBD, DNA-binding domain; ABD, actin-binding domain.