Figure 2.
RAP1A and RAP1B contribute to platelet integrin activation. Flow cytometric analysis of integrin αIIbβ3 activation (binding of Jon/A-PE; clone Leo.H4; Emfret Analytics) (A) and integrin β1 activation (binding of 9EG7–fluorescein isothiocyanate; BD Biosciences) (B) in response to increasing concentrations of thrombin, the GPVI-agonist convulxin, or the combination of ADP and the TxA2 analog U46619. Data shown are mean fluorescence intensity (MFI) ± SEM of control (Rap1afl/flRap1bfl/flPf4-Cre−), Rap1a-mKO (Rap1afl/flRap1bwt/wtPf4-Cre+), Rap1b-mKO (Rap1awt/wtRap1bfl/flPf4-Cre+), and Rap1a/b-mKO (Rap1afl/flRap1bfl/flPf4-Cre+) platelets (n = 6). *P < .05, **P < .01, ***P < .001. ns, not significant.

RAP1A and RAP1B contribute to platelet integrin activation. Flow cytometric analysis of integrin αIIbβ3 activation (binding of Jon/A-PE; clone Leo.H4; Emfret Analytics) (A) and integrin β1 activation (binding of 9EG7–fluorescein isothiocyanate; BD Biosciences) (B) in response to increasing concentrations of thrombin, the GPVI-agonist convulxin, or the combination of ADP and the TxA2 analog U46619. Data shown are mean fluorescence intensity (MFI) ± SEM of control (Rap1afl/flRap1bfl/flPf4-Cre−), Rap1a-mKO (Rap1afl/flRap1bwt/wtPf4-Cre+), Rap1b-mKO (Rap1awt/wtRap1bfl/flPf4-Cre+), and Rap1a/b-mKO (Rap1afl/flRap1bfl/flPf4-Cre+) platelets (n = 6). *P < .05, **P < .01, ***P < .001. ns, not significant.

Close Modal
This Feature Is Available To Subscribers Only

or Create an Account

Close Modal
Close Modal