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. Author manuscript; available in PMC: 2009 Oct 27.
Published in final edited form as: J Cell Sci. 2008 Sep 15;121(Pt 18):3071–3082. doi: 10.1242/jcs.031575

Fig. 2.

Fig. 2

c-Abl regulates filopodium formation during attachment through the interaction of PxxP motifs with Crk and Nck family proteins. A, B, and C. NIH3T3 cells were infected with control retrovirus (derived from pSUPER vector) or the one carrying shRNA sequence targeting CrkI/II/L or Nck1/2. These knockdown cells were super-infected with control retrovirus (derived from MIGR-1 vector) or virus expressing shRNA-resistant (human) CrkII or Nck2. D, E, and F. NIH3T3 cells overexpressing c-Abl, Nck2, or CrkII were treated with or without STI-571. A and D. Protein expression was examined by western blotting. B and F. Serum-starved cells were plated on coverslips coated with 10 μg/ml fibronectin, fixed at 20 minutes after plating, and stained for F-actin and DNA. White bars = 20 μm. C and E. The number of filopodia was counted from the fixed cells. Graph represents mean and/or S.E.M. of filopodia per cell or percentage of cells showing filopodia per total cells. ‡ indicates P<0.05, and ¶ indicates P=0.143.