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Integrating cardiac PIP3 and cAMP signaling through a PKA anchoring function of p110γ.

Abstract：

: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(3) production. This provides local feedback control of PIP(3) 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.

journal_name

Mol Cell

journal_title

Molecular cell

authors

Perino A,Ghigo A,Ferrero E,Morello F,Santulli G,Baillie GS,Damilano F,Dunlop AJ,Pawson C,Walser R,Levi R,Altruda F,Silengo L,Langeberg LK,Neubauer G,Heymans S,Lembo G,Wymann MP,Wetzker R,Houslay MD,Iaccarino G,S

doi

10.1016/j.molcel.2011.01.030

subject

Has Abstract

pub_date

2011-04-08 00:00:00

pages

84-95

issue

1

eissn

1097-2765

issn

1097-4164

pii

S1097-2765(11)00164-X

journal_volume

42

pub_type

杂志文章

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