Figure 7.
Figure 7. DGKζ deficiency enhances signaling in response to GPVI activation. WT and DGKζ-KO washed platelets were stimulated with 1 μg/mL of CRP for 90 and 300 seconds under stirring conditions in an aggregometer. Lysates were analyzed for DGKζ, phosphorylated ERK (P-ERK; Thr202/Tyr204), ERK2, P-Lyn (Tyr 507), Lyn, P-PLCγ2 (Tyr 1217), PLCγ2, P-Akt (Thr 308), Akt, and actin. (A) Blot shown is representative of 3 independent experiments. (B) Quantification of band densities normalized to actin over all experiments is reported as the mean ± SEM (n = 3). Statistical analysis was performed using the unpaired Student t test. *P < .05, **P < .01, ****P < .0001 of DGKζ-KO as compared with WT platelets.

DGKζ deficiency enhances signaling in response to GPVI activation. WT and DGKζ-KO washed platelets were stimulated with 1 μg/mL of CRP for 90 and 300 seconds under stirring conditions in an aggregometer. Lysates were analyzed for DGKζ, phosphorylated ERK (P-ERK; Thr202/Tyr204), ERK2, P-Lyn (Tyr 507), Lyn, P-PLCγ2 (Tyr 1217), PLCγ2, P-Akt (Thr 308), Akt, and actin. (A) Blot shown is representative of 3 independent experiments. (B) Quantification of band densities normalized to actin over all experiments is reported as the mean ± SEM (n = 3). Statistical analysis was performed using the unpaired Student t test. *P < .05, **P < .01, ****P < .0001 of DGKζ-KO as compared with WT platelets.

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