Fig. 3: The thrombin-PKC pathway engages Src to phosphorylate C3G at Tyr504.
From: C3G contributes to platelet activation and aggregation by regulating major signaling pathways
a tgC3G platelets, tgC3GΔCat platelets and their controls (wtC3G and wtC3GΔCat, respectively) were treated with thrombin (0.5 U/ml) in the presence or absence of PP2 (10 μM) and labeled with anti-pTyr418-Src_Cy3 (green) and anti-pTyr504-C3G_Cy5 (red). Upper left: representative immunofluorescence confocal microscopy images of platelets of each genotype under each treatment condition taken at the same exposure time. Bar: 2 μm. Histograms represent the mean ± SD of the fluorescence intensities (arbitrary units) of pTyr504-C3G (p-C3G, upper right panels) and pTyr418-Src (p-Src, lower panels), as quantified by ImageJ. T: thrombin. b tgC3G platelets, tgC3GΔCat platelets and their controls were stimulated with PMA (2 μM) in the presence or absence of BIS (5 μM) and labeled with anti-pTyr418-Src_Cy5 (red) and phalloidin (green). Left: representative immunofluorescence confocal microscopy images of platelets of each genotype under each treatment condition taken at the same exposure time. Bar: 2 μm. Right: histograms represent the mean ± SD of the fluorescence intensity (arbitrary units) of p-Src relative to the phalloidin signal, as quantified by ImageJ. *p < 0.05, **p < 0.01, ***p < 0.001. tg: transgenic; wt: wild-type; BIS: bisindolylmaleimide.
