Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
Research Program Projects (P01)
Project #
5P01HL028001-11
Application #
3844131
Study Section
Project Start
Project End
Budget Start
Budget End
Support Year
11
Fiscal Year
1992
Total Cost
Indirect Cost
Name
University of Vermont & St Agric College
Department
Type
DUNS #
066811191
City
Burlington
State
VT
Country
United States
Zip Code
05405
Peterson, J N; Nassar, R; Anderson, P A et al. (2001) Altered cross-bridge characteristics following haemodynamic overload in rabbit hearts expressing V3 myosin. J Physiol 536:569-82
Peterson, J N; Alpert, N R (1998) Cross-bridge dynamics in the contracting heart. Adv Exp Med Biol 453:117-23;discussion 123-4
Alpert, N R; Mulieri, L A (1997) Human heart failure: determinants of ventricular dysfunction. Adv Exp Med Biol 430:97-108
Peterson, J N; Alpert, N R (1996) Molecular motor mechanics in the contracting heart. V1 versus V3 myosin heavy chain. Ann N Y Acad Sci 793:54-63
VanBuren, P; Harris, D E; Alpert, N R et al. (1995) Cardiac V1 and V3 myosins differ in their hydrolytic and mechanical activities in vitro. Circ Res 77:439-44
Haeberle, J R (1994) Calponin decreases the rate of cross-bridge cycling and increases maximum force production by smooth muscle myosin in an in vitro motility assay. J Biol Chem 269:12424-31
Zarain-Herzberg, A; Marques, J; Sukovich, D et al. (1994) Thyroid hormone receptor modulates the expression of the rabbit cardiac sarco (endo) plasmic reticulum Ca(2+)-ATPase gene. J Biol Chem 269:1460-7
Laporte, R; Haeberle, J R; Laher, I (1994) Phorbol ester-induced potentiation of myogenic tone is not associated with increases in Ca2+ influx, myoplasmic free Ca2+ concentration, or 20-kDa myosin light chain phosphorylation. J Mol Cell Cardiol 26:297-302
Hemric, M E; Tracy, P B; Haeberle, J R (1994) Caldesmon enhances the binding of myosin to the cytoskeleton during platelet activation. J Biol Chem 269:4125-8
Fisher, S A; Periasamy, M (1994) Collagen synthesis inhibitors disrupt embryonic cardiocyte myofibrillogenesis and alter the expression of cardiac specific genes in vitro. J Mol Cell Cardiol 26:721-31

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