Moreover, in a subset of end-stage failing patient hearts showing increased CaMKIIδ expression and activity, N2Bus sites p-S4010 (PKA/ERK2-dependent) and p-S4062 (CaMKIIδ-dependent) were hyper-phosphorylated compared to non-failing donor hearts, as was PEVK site p- S11878 (PKCα-dependent), whereas p- S12022 (CaMKIIδ/PKCα-dependent) showed a trend for increased phosphorylation and p-S4099 (PKG-dependent) remained unaltered (Hamdani et al. 2013c ).
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Tampering with springs: phosphorylation of titin affecting the mechanical function of cardiomyocytes.
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