8 research outputs found
Atoms interacting with intense, high-frequency laser pulses: Effect of the magnetic-field component on atomic stabilization
Published versio
Direct top-down fabrication of nanoscale electrodes for organic semiconductors using fluoropolymer resists
Phosphorus Availability Bioassay Using Bone Ash and Bone Densitometry as Response Criteria
Integrating cardiac PIP<sub>3</sub> and cAMP signaling through a PKA anchoring function of p110γ
Adrenergic stimulation of the heart engages cAMP and phosphoinositide second messenger signaling cascades. Cardiac phosphoinositide 3-kinase p110γ participates in these processes by sustaining β-adrenergic receptor internalization through its catalytic function and by controlling phosphodiesterase 3B (PDE3B) activity via an unknown kinase-independent mechanism. We have discovered that p110γ anchors protein kinase A (PKA) through a site in its N-terminal region. Anchored PKA activates PDE3B to enhance cAMP degradation and phosphorylates p110γ to inhibit PIP<sub>3</sub> production. This provides local feedback control of PIP<sub>3</sub> and cAMP signaling events. In congestive heart failure, p110γ is upregulated and escapes PKA-mediated inhibition, contributing to a reduction in β-adrenergic receptor density. Pharmacological inhibition of p110γ normalizes β-adrenergic receptor density and improves contractility in failing hearts