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. Author manuscript; available in PMC: 2012 Jan 15.
Published in final edited form as: Cancer Res. 2011 Jan 11;71(2):360–370. doi: 10.1158/0008-5472.CAN-10-2894

Figure 2.

Figure 2

Gastrin stimulates FA formation, translocation of FAK to FAs, and the formation of an Rgnef-FAK-paxillin complex. A, Rgnef, FAK, and Pyk2 expression compared to β-actin in human colon carcinoma cell lines as determined by immunoblotting. B, Pharmacological FAK inhibitor addition (PF-228, 1 μM) blocks gastrin-stimulated FAK and paxillin tyrosine phosphorylation as determined by immunoprecipitation (IP) and immunoblotting. C, Serum-starved DLD-1 colonies were stimulated by gastrin or DMSO (control) addition and after 60 min, processed for immunostaining. Paxillin (FA marker) was in a punctate cytoplasmic distribution in DMSO-treated cells and upon gastrin stimulation, increased paxillin staining at peripheral cell projections and at cell-cell junctions (arrows) was observed that were also sites of filamentous actin accumulation. Cell nuclei were visualized with DAPI. Accumulation of FAK staining at peripheral FAs upon gastrin addition to DLD-1 cells. Scale bar is 10 μm. D, Rgnef-FAK complex formation in DLD-1 cells as determined by co-IP with antibodies to FAK and Rgnef and reciprocal immunoblotting. Gastrin stimulates increased FAK-paxillin association. Antibodies to FAK co-IP Rgnef and paxillin after gastrin addition.