J. Hopkins

Cardiac hypertrophy with preserved contractile function after selective deletion of GLUT4 from the heart.

B. Lowell, T. Doetschman, J. Ingwall, 1999, The Journal of clinical investigation.

Kinetic, Thermodynamic, and Developmental Consequences of Deleting Creatine Kinase Isoenzymes from the Heart

J. Ingwall, M. Spindler, K. Saupe, 2000, The Journal of Biological Chemistry.

Type 2 Iodothyronine Deiodinase Transgene Expression in the Mouse Heart Causes Cardiac-Specific Thyrotoxicosis**This work was supported by grants from the NIH [DK-36256 (to P.R.L.); DK-49126 and DK-53036 (to F.E.W.) and Specialized Center of Research Grant HL-52320 (to J.S.I.)].

P. Larsen, J. Ingwall, R. Peeters, 2001, Endocrinology.

Control of cardiac energetics: from models to human disease

G. Radda, K. Clarke, J. Hopkins, 2000, Magma: Magnetic Resonance Materials in Physics, Biology, and Medicine.

Role of MgADP in the development of diastolic dysfunction in the intact beating rat heart.

J. Halow, S. A. Camacho, J. Ingwall, 1997, The Journal of clinical investigation.

Muscular dystrophy: from gene to patient

G. Radda, K. Davies, K. Clarke, 2000, Magma: Magnetic Resonance Materials in Physics, Biology, and Medicine.

Type 2 iodothyronin deiodinase transgene expression in the mouse heart causes cardiac-specific thyrotoxicosis.

P. Larsen, J. Ingwall, R. Peeters, 2001, Endocrinology.

Accumulation of 2-deoxy-D-glucose-6-phosphate as a measure of glucose uptake in the isolated perfused heart: a 31P NMR study.

G. Radda, K. Clarke, R. Veech, 2004, Metabolic engineering.