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. 2011 Mar 28;286(22):20100–20108. doi: 10.1074/jbc.M111.220236

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© 2011 by The American Society for Biochemistry and Molecular Biology, Inc.

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FIGURE 4. — Roles of PKA and CaMKII in ER Ca²⁺ release-induced eNOS Ser-635 phosphorylation. BAECs were pretreated with PKA or CaMKII inhibitors for 15 min and then subjected to TG stimulation. A, effects of PKA inhibition on ER Ca²⁺ release-induced eNOS Ser-635 phosphorylation. As shown, PKA inhibitor H89 (10 μm) or PKI (10 μm) had no significant effect on the increases of eNOS Ser-635 phosphorylation in TG-treated cells. Representative data are shown from three independent experiments. B, quantitative analyses of the effects of PKA inhibitors on ER Ca²⁺ release-induced eNOS Ser-635 phosphorylation. The data are shown as the means ± S.E. (n = 3). C, effects of CaMKII inhibitor KN93 (50 μm) and the inactive control compound KN92 (50 μm) on ER Ca²⁺ release-induced eNOS Ser-635 phosphorylation. D, quantitative analyses of the effects of CaMKII inhibition on ER Ca²⁺ release-induced eNOS Ser-635 phosphorylation (n = 3).