Phosphodieasterase 4 and phosphatase 2A differentially regulate cAMP/PKA signaling for cardiac myocyte contraction under stimulation of β1 adrenergic receptor

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  Figure S1. (A) Inhibition of PDE4 with rolipram and inhibition of PP2A with okadaic acid did not change the cell surface density of N-terminal HA tagged β1AR expressed on β1β2AR-KO cardiac myocytes. (B) Inhibition of PP2A with okadaic acid did not change the basal level cAMP in β2AR-KO cardiac myocytes, nor did it significantly change cAMP accumulation after stimulation with 10-5M isoproterenol.
  Figure S2. Inhibition of PDE3 or PKA disrupts rhythmic contraction in adult cardiac myocytes. (A) Inhibition of PDE3 with cilostamide (cilo) disrupts rhythmic contraction in β2AR-KO myocytes. The myocytes display increased contraction frequencies (see low panel for detail). (B) Inhibition of PKA with PKI disrupts rhythmic contraction in β2ARKO myocytes. The myocytes display decreases in both shortening and contraction frequencies.