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. Author manuscript; available in PMC: 2019 Aug 1.
Published in final edited form as: J Mol Cell Cardiol. 2018 Jun 7;121:51–59. doi: 10.1016/j.yjmcc.2018.06.002

Figure 7. Model for control of PI4P hydrolysis by distinct inputs to PLCε signaling.

Figure 7

In this model, β-adrenergic receptor stimulation of adenylyl cyclase (AC) generates pools of cAMP that are differentially regulated by PDE2 and PDE3. PDE3 limits the ability of cAMP to activate Epac-PLCε, while PDE2 limits cAMP dependent inhibition of PLCε through PKA. Similarly, cGMP generated by activation of guanylyl cyclase (GC) inhibits PLCε through PKG activation, but this pathway may be indirect, as indicated by the dashed lines. PDE9 and possible PDE2 limit the ability of cGMP to act on this inhibitory PKG-dependent pathway.