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. Author manuscript; available in PMC: 2022 Feb 19.
Published in final edited form as: Circ Res. 2020 Dec 18;128(4):455–470. doi: 10.1161/CIRCRESAHA.120.318409

Figure 3.

Figure 3.

JNK2 increases the maximal rate of SERCA2-ATPases activity. A) Summarized data showing alcohol exposure (0.23%, 24hr) increases thapsigargin (TG)-sensitive SERCA2-ATPase activity in isolated human atrial SR vesicles, but the treatment of JNK2-specific inhibitor (JNK2I) attenuates the alcohol-enhanced SERCA2-ATPase activity. JNK2I (170 nM) treatment shows no inhibitory effect on the baseline activity of SERCA2 in sham human atrial SR vesicles. B-C) pooled data of Ca2+-dependent curves of SERCA2-ATPase activity (B) and Ca2+ affinity (Km, C) in human atrial SR vesicles incubated with pure active hJNK2 (64ng) at reaction times of 10 (green), 20 (blue), 30 (pink), and 60 (red) min compared to sham controls (black). And summarized data showing suppressed Ca2+-dependent responses of SERCA2-ATPase activities by incubating with 0.5 μM thapsigargin (brown open squares) compared to sham controls (black dots). E) Pooled data of time-dependent phosphorylation of hSERCA2-PN by 10 ng pure active hJNK2 (10 μM Ca2+).