Fig. 5.
Fig. 5. Platelets form Vav1-  and Vav1/Vav2-deficient mice spread normally on fibrinogen. / (A) Wild-type platelets were spread on a fibrinogen monolayer for 30 minutes in the presence of (i) DMSO, (ii) apyrase (2 U/mL) and indomethacin (10 μM), or (iii) the Src family kinase inhibitor PP2 (20 μM). Slides were stained with rhodamine phalloidin and imaged by fluorescence microscopy. (B) The ability of wild-type, Vav1−/−, and Vav1−/−Vav2−/−mouse platelets to spread on fibrinogen-coated coverslips was studied by labeling of F-actin with rhodamine phalloidin followed by fluorescence microscopy. The surface area of spread platelets was measured at 30 minutes. Data are shown as mean surface area plus SEM. One experiment representative of 3 is depicted.

Platelets form Vav1-  and Vav1/Vav2-deficient mice spread normally on fibrinogen.

(A) Wild-type platelets were spread on a fibrinogen monolayer for 30 minutes in the presence of (i) DMSO, (ii) apyrase (2 U/mL) and indomethacin (10 μM), or (iii) the Src family kinase inhibitor PP2 (20 μM). Slides were stained with rhodamine phalloidin and imaged by fluorescence microscopy. (B) The ability of wild-type, Vav1−/−, and Vav1−/−Vav2−/−mouse platelets to spread on fibrinogen-coated coverslips was studied by labeling of F-actin with rhodamine phalloidin followed by fluorescence microscopy. The surface area of spread platelets was measured at 30 minutes. Data are shown as mean surface area plus SEM. One experiment representative of 3 is depicted.

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