• Publications
  • Influence
The role of phosphoinositide-3 kinase and PTEN in cardiovascular physiology and disease.
Phosphoinositide-3 kinases (PI3Ks) are a family of evolutionary conserved lipid kinases that mediate many cellular responses in both physiologic and pathophysiologic states. Class I PI3K can beExpand
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PI3K&ggr; Is Required for PDE4, not PDE3, Activity in Subcellular Microdomains Containing the Sarcoplasmic Reticular Calcium ATPase in Cardiomyocytes
We recently showed that phosphoinositide-3-kinase-&ggr;–deficient (PI3K&ggr;−/−) mice have enhanced cardiac contractility attributable to cAMP-dependent increases in sarcoplasmic reticulum (SR) Ca2+Expand
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Mineralocorticoid Receptor Antagonism Prevents the Electrical Remodeling That Precedes Cellular Hypertrophy After Myocardial Infarction
Background—Cardiac hypertrophy underlies arrhythmias and sudden death, for which mineralocorticoid receptor (MR) activity has recently been implicated. We sought to establish the sequence of ionicExpand
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Tachycardia-induced silencing of subcellular Ca2+ signaling in atrial myocytes.
Atrial fibrillation (AF) is characterized by sustained high atrial activation rates and arrhythmogenic cellular Ca2+ signaling instability; however, it is not clear how a high atrial rate and Ca2+Expand
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  • Open Access
Insulin-like growth factor-1 and PTEN deletion enhance cardiac L-type Ca2+ currents via increased PI3Kalpha/PKB signaling.
Ca2+ influx through the L-type Ca2+ channel (I(Ca,L)) is a key determinant of cardiac contractility and is modulated by multiple signaling pathways. Because the regulation of I(Ca,L) byExpand
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Cardiac-specific elevations in thyroid hormone enhance contractility and prevent pressure overload-induced cardiac dysfunction.
Thyroid hormone (TH) is critical for cardiac development and heart function. In heart disease, TH metabolism is abnormal, and many biochemical and functional alterations mirror hypothyroidism.Expand
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  • Open Access
Insulin-Like Growth Factor-1 and PTEN Deletion Enhance Cardiac L-Type Ca2+ Currents via Increased PI3Kα/PKB Signaling
Ca2+ influx through the L-type Ca2+ channel (ICa,L) is a key determinant of cardiac contractility and is modulated by multiple signaling pathways. Because the regulation of ICa,L byExpand
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Cardiac Sarcoplasmic Reticulum Calcium Release and Load Are Enhanced by Subcellular cAMP Elevations in PI3K&ggr;-Deficient Mice
We recently showed that phosphoinositide-3-kinase-&ggr;–deficient (PI3K&ggr;−/−) mice have increased cardiac contractility without changes in heart size compared with control mice (ie, PI3K&ggr;+/+Expand
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Phosphoinositide 3-kinase gamma regulates cardiac contractility by locally controlling cyclic adenosine monophosphate levels.
Class I phosphoinositide 3-kinases (PI3Ks) are enzymes with both protein and lipid kinase activities that regulate important cellular functions in many tissues. In the heart, subclass IA PI3KsExpand
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  • Open Access
Rabbit, a relevant model for the study of cardiac β3‐adrenoceptors
The β3‐adrenoceptors (β3‐ARs) have been identified and characterized in the human heart. Specific β3‐AR stimulation, unlike β1‐AR or β2‐AR stimulation, decreases cardiac contractility, partly via theExpand
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