Figure 6
Figure 6. Early agonist induced signaling is unaffected by the absence of ILK. PLCγ2 immunoprecipitated from ILK-deficient and control (Ctrl) washed platelets was prepared from resting and collagen-stimulated (100 μg/mL 90 seconds) samples. Samples were immunoblotted for tyrosine phosphorylation, stripped, and reprobed for PLCγ2 loading levels, and densitometric analysis was carried out (A; mean ± SEM, n = 3; P = .44). A representative blot of PLCγ2 and tyrosine phosphorylation (4G10) levels is shown (B). Calcium mobilization in Fluo-4AM– labeled control (Ctrl) and ILK-deficient platelets was monitored in a Flexstation II, and change in fluorescence was expressed as the percentage increase in calcium from resting levels (mean ± SEM, n = 3; P = .16; C).

Early agonist induced signaling is unaffected by the absence of ILK. PLCγ2 immunoprecipitated from ILK-deficient and control (Ctrl) washed platelets was prepared from resting and collagen-stimulated (100 μg/mL 90 seconds) samples. Samples were immunoblotted for tyrosine phosphorylation, stripped, and reprobed for PLCγ2 loading levels, and densitometric analysis was carried out (A; mean ± SEM, n = 3; P = .44). A representative blot of PLCγ2 and tyrosine phosphorylation (4G10) levels is shown (B). Calcium mobilization in Fluo-4AM– labeled control (Ctrl) and ILK-deficient platelets was monitored in a Flexstation II, and change in fluorescence was expressed as the percentage increase in calcium from resting levels (mean ± SEM, n = 3; P = .16; C).

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