Heart Institute

Marjorie Maillet, PhD

Title

Research Fellow, Division of Molecular Cardiovascular Biology

Email

marjorie.maillet@cchmc.org

Phone

513-636-2467

Awards and Honors

Post-Doc Fellow, HHMI, 2008.
Post-Doctoral Fellowship from the Ohio Valley Affiliate branch of the American Heart Association (0625282B), 2006-2008.
Young Investigator Travel Award, AHA meeting, Keystone, Colorado, 2006.

Research

Cardiovascular signaling

Publications, Most Recent

Maillet, M., Purcell, N. H., Sargent, M. A., York, A. J., Bueno, O. F. and Molkentin, J. D. DUSP6 (MKP3) Null Mice Show Enhanced ERK1/2 Phosphorylation at Baseline and Increased Myocyte Proliferation in the Heart Affecting Disease Susceptibility. J. Biol. Chem., 2008; 283, 31246-55.

Oka, T., Maillet, M., Watt, A. J., Schwartz, R. J., Aronow, B. J., Duncan, S. A. and Molkentin, J. D. Cardiac-specific deletion of Gata4 reveals its requirement for hypertrophy, compensation, and myocyte viability. Circ. Res., 2006; 98, 837-45.

Presentations, Most Recent

Maillet M., Purcell N. H., Sargent M. A., York A., Bueno O. F., Molkentin J. D. Enhanced ERK1/2 phosphorylation at baseline in Dusp6 null mice increases cardiomyocyte proliferation and antagonizes heart disease. ISHR North American Section Meeting, Cincinnati, Ohio, June 17-20; 2008.

Maillet M., Sanna B., Zheng Y., Molkentin J. D. Cardiac-Specific Deletion of the Small Rho GTPase Cdc42 Shows its Function as an Anti-Hypertrophic Effector. AHA meeting, Orlando, Florida, November 9-12; 2007. (Oral communication)

Maillet M., Sanna B., Zheng Y., Molkentin J. D. Cardiac-Specific Deletion of the Small Rho GTPase Cdc42 Reveals Its Pivotal Function in Cardiac Hypertrophy. AHA meeting, Keystone, Colorado, July,August 31-3rd , 2006.