Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
Research Project (R01)
Project #
2R01HL061558-07
Application #
6725298
Study Section
Cardiovascular and Pulmonary Research A Study Section (CVA)
Program Officer
Buxton, Denis B
Project Start
1999-01-11
Project End
2004-08-31
Budget Start
2004-01-01
Budget End
2004-08-31
Support Year
7
Fiscal Year
2004
Total Cost
$214,628
Indirect Cost
Name
Duke University
Department
Internal Medicine/Medicine
Type
Schools of Medicine
DUNS #
044387793
City
Durham
State
NC
Country
United States
Zip Code
27705
Yoo, ByungSu; Lemaire, Anthony; Mangmool, Supachoke et al. (2009) Beta1-adrenergic receptors stimulate cardiac contractility and CaMKII activation in vivo and enhance cardiac dysfunction following myocardial infarction. Am J Physiol Heart Circ Physiol 297:H1377-86
Volovyk, Zoya M; Wolf, Matthew J; Prasad, Sathyamangla V Naga et al. (2006) Agonist-stimulated beta-adrenergic receptor internalization requires dynamic cytoskeletal actin turnover. J Biol Chem 281:9773-80
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Naga Prasad, Sathyamangla V; Laporte, Stephane A; Chamberlain, Dean et al. (2002) Phosphoinositide 3-kinase regulates beta2-adrenergic receptor endocytosis by AP-2 recruitment to the receptor/beta-arrestin complex. J Cell Biol 158:563-75
Harding, V B; Jones, L R; Lefkowitz, R J et al. (2001) Cardiac beta ARK1 inhibition prolongs survival and augments beta blocker therapy in a mouse model of severe heart failure. Proc Natl Acad Sci U S A 98:5809-14
Kohout, T A; Takaoka, H; McDonald, P H et al. (2001) Augmentation of cardiac contractility mediated by the human beta(3)-adrenergic receptor overexpressed in the hearts of transgenic mice. Circulation 104:2485-91

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