β-Arrestin–dependent activation of Ca2+/calmodulin kinase II after β1–adrenergic receptor stimulation

β1-Adrenergic receptors stimulate cardiac contractility and CaMKII activation in vivo and enhance cardiac dysfunction following myocardial infarction

(2009) ByungSu Yoo et al.   AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY

CaMKII and a failing strategy for growth in heart

(2009) Mark E. Anderson   JOURNAL OF CLINICAL INVESTIGATION

Requirement for Ca2+/calmodulin–dependent kinase II in the transition from pressure overload–induced cardiac hypertrophy to heart failure in mice

(2009) Haiyun Ling et al.   JOURNAL OF CLINICAL INVESTIGATION

Direct Spatial Control of Epac1 by Cyclic AMP

(2009) B. Ponsioen et al.   MOLECULAR AND CELLULAR BIOLOGY

Epac Mediates β-Adrenergic Receptor–Induced Cardiomyocyte Hypertrophy

(2008) Mélanie Métrich et al.   CIRCULATION RESEARCH

Epac and Phospholipase Cϵ Regulate Ca2+Release in the Heart by Activation of Protein Kinase Cϵ and Calcium-Calmodulin Kinase II

(2008) Emily A. Oestreich et al.   JOURNAL OF BIOLOGICAL CHEMISTRY

Physical Interaction of Calmodulin with the 5-Hydroxytryptamine2C Receptor C-Terminus Is Essential for G Protein-independent, Arrestin-dependent Receptor Signaling

(2008) Marilyne Labasque et al.   MOLECULAR BIOLOGY OF THE CELL

Distinct conformational changes in  -arrestin report biased agonism at seven-transmembrane receptors

(2008) A. K. Shukla et al.   PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA