Fig. 6.

Model for roles of Abl, Crk, and Nck in cell spreading. Integrin engagement increases catalytic activity of c-Abl. Due to interaction of Abl PxxP motifs 1, 2, and 4 with CrkII, active c-Abl phosphorylates and inactivates CrkII (colored in grey), 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 c-Abl catalytic activity is low, CrkII remains active and promotes focal adhesion formation and Rac1 activation, resulting in increased formation of lamellipodia. c-Abl and Nck no longer productively interact and transduce signals (Nck under this situation is colored in grey). As a result, low c-Abl activity decreases filopodium formation and accelerates spreading speed of cells.