Mice lacking the signaling molecule CalDAG-GEFI represent a model for leukocyte adhesion deficiency type III
J. Clin. Invest. Wolfgang Bergmeier, et al. 117:1699 doi:10.1172/JCI30575 [Go to this article.]

Figure 6
Impaired activation of β₁ integrins in CalDAG-GEFI–deficient platelets. (A and B) Biotinylated WT and CalDAG-GEFI–deficient platelets were stimulated with PAR4p (2 mM) or U46619/ADP (5 or 10 μM) in the presence of a blocking antibody to α_IIbβ₃ and allowed to adhere for 30 minutes under static conditions to laminin (A) or fibronectin (B) in microtiter plates. A separate group of WT platelets was pretreated with a blocking antibody to α₆ (adhesion to laminin) or with EDTA (adhesion to fibronectin) to demonstrate the integrin dependency of the adhesion process. Adherent platelets were quantified colorimetrically for peroxidase activity. Data are mean ± SEM of 3 individual experiments in triplicate wells. **P < 0.01, ***P < 0.001. Similar results were observed with nonbiotinylated platelets when the number of adhesive platelets was determined by light microscopy (not shown).