Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
Specialized Center (P50)
Project #
5P50HL052320-05
Application #
6110367
Study Section
Project Start
1999-01-01
Project End
1999-12-31
Budget Start
1998-10-01
Budget End
1999-09-30
Support Year
5
Fiscal Year
1999
Total Cost
Indirect Cost
Name
Brigham and Women's Hospital
Department
Type
DUNS #
071723621
City
Boston
State
MA
Country
United States
Zip Code
02115
Herman, Daniel S; Lam, Lien; Taylor, Matthew R G et al. (2012) Truncations of titin causing dilated cardiomyopathy. N Engl J Med 366:619-28
Alcalai, Ronny; Wakimoto, Hiroko; Arad, Michael et al. (2011) Prevention of ventricular arrhythmia and calcium dysregulation in a catecholaminergic polymorphic ventricular tachycardia mouse model carrying calsequestrin-2 mutation. J Cardiovasc Electrophysiol 22:316-24
Pinz, Ilka; Zhu, Ming; Mende, Ulrike et al. (2011) An improved isolation procedure for adult mouse cardiomyocytes. Cell Biochem Biophys 61:93-101
Shen, Weiqun; Vatner, Dorothy E; Vatner, Stephen F et al. (2010) Progressive loss of creatine maintains a near normal DeltaG approximately (ATP) in transgenic mouse hearts with cardiomyopathy caused by overexpressing Gsalpha. J Mol Cell Cardiol 48:591-9
Saltzman, Adam J; Mancini-DiNardo, Debora; Li, Chumei et al. (2010) Short communication: the cardiac myosin binding protein C Arg502Trp mutation: a common cause of hypertrophic cardiomyopathy. Circ Res 106:1549-52
Gnecchi, Massimiliano; He, Huamei; Melo, Luis G et al. (2009) Early beneficial effects of bone marrow-derived mesenchymal stem cells overexpressing Akt on cardiac metabolism after myocardial infarction. Stem Cells 27:971-9
Pinz, Ilka; Ostroy, Sanford E; Hoyer, Kirsten et al. (2008) Calcineurin-induced energy wasting in a transgenic mouse model of heart failure. Am J Physiol Heart Circ Physiol 294:H1459-66
Pinz, Ilka; Robbins, Jeffrey; Rajasekaran, Namakkal S et al. (2008) Unmasking different mechanical and energetic roles for the small heat shock proteins CryAB and HSPB2 using genetically modified mouse hearts. FASEB J 22:84-92
Pinz, Ilka; Wax, Stephen D; Anderson, Paul et al. (2008) Low over-expression of TNFalpha in the mouse heart increases contractile performance via TNFR1. J Cell Biochem 105:99-107
Hoyer, Kirsten; Krenz, Maike; Robbins, Jeffrey et al. (2007) Shifts in the myosin heavy chain isozymes in the mouse heart result in increased energy efficiency. J Mol Cell Cardiol 42:214-21

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