Fig. 6. Model for roles of Abl, Crk and Nck in cell spreading. Integrin engagement increases catalytic activity of Abl. Owing to interaction of Abl PxxP motifs 1, 2 and 4 with CrkII, active Abl phosphorylates and inactivates CrkII (gray), together with interaction between PxxP motif 3 and Nck, inhibiting focal adhesion formation and Rac1 activation and thus decreasing lamellipodium formation. These actions also cause increased filopodium formation and eventually slow cell spreading. When Abl catalytic activity is low, CrkII remains active and promotes focal adhesion formation and Rac1 activation, resulting in increased formation of lamellipodia. Abl and Nck no longer productively interact and transduce signals (gray). As a result, low Abl activity decreases filopodium formation and accelerates spreading speed of cells.