Fig. 2.

Schematic depiction of the functional domains of human (1a and 1b) and murine (I and IV) Abl isoforms. The N terminus of c-Abl contains either an autoinhibitory Cap region or a consensus motif for myristoylation (black), which is followed by SH3 (blue; colors refer to the online version only) and SH2 (pink) domains, which is followed by the catalytic PTK domain (kinase, yellow). The central region of c-Abl possesses 4 PXXPXK/R sequences (purple), 3 nuclear localization sequences (NLS, white), and 3 high-mobility group-like boxes (HLB, green). Finally, the C terminus of c-Abl houses domains for binding globular (G, orange) and filamentous (F, gray) actin, as well as a nuclear export sequence (NES, brown). The oncogenic forms of Abl (v-Abl and BCR-Abl) contain modified N-terminal regions that disrupt the autoinhibitory functions normally mediated by the Cap region, which elicits constitutive PTK activity. The aberrant N terminus in v-Abl comprises a viral Gag sequence (light blue), while that in BCR-Abl comprises a portion of the N terminus of the BCR (red).