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. 1998 Mar 1;12(5):667–678. doi: 10.1101/gad.12.5.667

Figure 6.

Figure 6

 EphB1/Fc blocks juxtacrine activation of EphB1 and EphB2 by PMA and blocks capillary-like endothelial assembly. (A) HRMEC were plated on Matrigel-coated 35-mm dishes and stimulated as above with agonists added in the absence (−) or presence (+) or a competitive EphB1 ectodomain antagonist, EphB1/Fc (500 ng/ml). As before, EphB1 immunoprecipitates were analyzed for receptor recovery (anti-EphB1), activation (anti-pTyr, 130kD), and recruitment of LMW–PTP (anti-pTyr and anti-LMW–PTP, 18 kD). EphB1/Fc blocked the PMA-stimulated EphB1 activation and LMW–PTP recruitment. (B) EphB1 (left) or EphB2 (right) immunoprecipitates were recovered from HRMEC plated on Matrigel at high density and stimulated for 15 min with no addition (NA), PMA (20 ng/ml), or preclustered ephrin-B1/Fc (250 ng/ml) plus anti-Fc (25 ng/ml), as above, in the absence (−) or presence (+) or EphB1/Fc (500 ng/ml). (C) Cells were plated as in Fig. 1 in medium containing no addition (no addition), PMA (20 ng/ml) or preclustered ephrin-B1/Fc (250 ng/ml) plus anti-Fc (25 ng/ml), in the absence (NA) or presence (+EphB1/Fc, 500 ng/ml) of receptor ectodomain competitor. EphB1/Fc blocked capillary-like endothelial assembly responses to PMA and clustered ephrin-B1/Fc.