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. Author manuscript; available in PMC: 2015 Aug 1.
Published in final edited form as: J Heart Lung Transplant. 2014 Mar 5;33(8):785–793. doi: 10.1016/j.healun.2014.02.030

Figure 6.

Figure 6

Phosphorylation of the calcium/calmodulin-dependent protein kinase (CaMK) target site on phospholamban (PLB), threonine 17 (PT17), is increased in decompensated hypoplastic left heart syndrome (D-HLHS) compared with the non-failing right ventricle (NF-RV). (A) By Western blot analysis, there was no difference in total PLB between HLHS (compensated [C]-HLHS, n = 9; D-HLHS, n = 9) and NF-RV (n = 9). (B) There was increased phosphorylation of PT17 in D-HLHS (n = 6) compared with NF-RV (n = 8) and C-HLHS (n = 10) (C) but no differences in phosphorylation of PLB at the protein kinase A (PKA) target site, Ser16, between groups (NF-RV, n = 9; C-HLHS, n = 10; and D-HLHS, n = 7). Results are presented as the mean with the standard error (error bars).