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Literature summary for 3.1.4.53 extracted from

  • Mika, D.; Richter, W.; Westenbroek, R.E.; Catterall, W.A.; Conti, M.
    PDE4B mediates local feedback regulation of beta1-adrenergic cAMP signaling in a sarcolemmal compartment of cardiac myocytes (2014), J. Cell Sci., 127, 1033-1042.
    View publication on PubMedView publication on EuropePMC
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Organism

Organism UniProt Comment Textmining
Mus musculus
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Source Tissue

Source Tissue Comment Organism Textmining
heart neonatal cardiac myocyte Mus musculus
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Synonyms

Synonyms Comment Organism
PDE4B
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 Mus musculus

General Information

General Information Comment Organism
physiological function isoform PDE4B is involved in beta-adrenergic signaling in the heart. Genetic ablation of PDE4B disrupts beta-adrenergic signaling-induced cAMP transients at the sarcolemma but not in the bulk cytosol of cardiomyocytes. PDE4B regulates beta1-adrenergic signaling-, but not beta2-adrenergic signaling- or PGE2-induced responses. PDE4B shows selective effects on protein kinase A-mediated phosphorylation patterns. PDE4B limits the proein kinase A-mediated phosphorylation of key players in excitation-contraction coupling that reside in the sarcolemmal compartment, including L-type Ca2+ channels and ryanodine receptors, but not phosphorylation of distal cytosolic proteins. beta1-Adrenergic signaling- but not beta2-adrenergic signaling-ligation induced protein kinase A-dependent activation of PDE4B and interruption of this negative feedback with protein kinase A inhibitors increase sarcolemmal cAMP Mus musculus