Julie R. McMullen
Beth Israel Deaconess Medical Center
Harvard Medical School
Boston
MA 02215
USA
Name/email consistency: high
- The insulin-like growth factor 1 receptor induces physiological heart growth via the phosphoinositide 3-kinase(p110alpha) pathway. McMullen, J.R., Shioi, T., Huang, W.Y., Zhang, L., Tarnavski, O., Bisping, E., Schinke, M., Kong, S., Sherwood, M.C., Brown, J., Riggi, L., Kang, P.M., Izumo, S. J. Biol. Chem. (2004)
- Inhibition of mTOR signaling with rapamycin regresses established cardiac hypertrophy induced by pressure overload. McMullen, J.R., Sherwood, M.C., Tarnavski, O., Zhang, L., Dorfman, A.L., Shioi, T., Izumo, S. Circulation (2004)
- Deletion of ribosomal S6 kinases does not attenuate pathological, physiological, or insulin-like growth factor 1 receptor-phosphoinositide 3-kinase-induced cardiac hypertrophy. McMullen, J.R., Shioi, T., Zhang, L., Tarnavski, O., Sherwood, M.C., Dorfman, A.L., Longnus, S., Pende, M., Martin, K.A., Blenis, J., Thomas, G., Izumo, S. Mol. Cell. Biol. (2004)
- Phosphoinositide 3-kinase(p110alpha) plays a critical role for the induction of physiological, but not pathological, cardiac hypertrophy. McMullen, J.R., Shioi, T., Zhang, L., Tarnavski, O., Sherwood, M.C., Kang, P.M., Izumo, S. Proc. Natl. Acad. Sci. U.S.A. (2003)