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. Author manuscript; available in PMC: 2018 Feb 1.
Published in final edited form as: Neurobiol Learn Mem. 2016 Aug 12;138:10–20. doi: 10.1016/j.nlm.2016.08.006

Figure 5. Computational modeling determines that protein phosphatase 1 is a potential mechanism suppressing PKA activity in small dendritic compartments and excess PKA substrate does not affect PKA signaling dynamics.

Figure 5

(A-C) The computational model defined in Fig. 3A was modified to include different concentrations of protein phosphatase 1 (PP1) and various concentrations of PKA substrate (molecule “X”). (A) cAMP transients were not affected by different concentrations of PP1 or X. (B) PKAc Released increases with greater concentrations of X but were unaffected by greater PP1. (C) The normalized phosphorylation status of PDE4 was not affected by different concentrations of X, but was reduced with greater concentrations of PP1.