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. Author manuscript; available in PMC: 2013 Sep 1.
Published in final edited form as: J Thromb Haemost. 2012 Sep;10(9):1849–1858. doi: 10.1111/j.1538-7836.2012.04864.x

Figure 4. Mutation of FVIIa residue T99 prevents Ixolaris inhibition of TF-FVIIa mediated PAR-2 cleavage and signaling.

Figure 4

(A) CHO-TF cells transiently expressing FLAG-hPAR-2 were incubated with 20 nM FVIIa WT or T99Y in the presence of 50 nM or 200 nM Ixolaris. Residual surface PAR-2 was measured after 1 h of incubation (mean ± S.D., n=3, ** p<0.01, unpaired t test). (B) MDA-MB-231mfp cells were stimulated with 10 nM FVIIa wt, the signaling-defective variant Q143N, or T99Y with enhanced PAR-2 signaling in the absence or in the presence of 200 nM Ixolaris for 90 min, and PAR-2 dependent IL-8 and CXCL-1 mRNA induction was quantified by RT-PCR (mean ± S.D., n=3, * p<0.05, unpaired t test, different from control).