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Julie R. McMullen

Beth Israel Deaconess Medical Center

Harvard Medical School

Boston

MA 02215

USA

[email]@*.harvard.edu

Name/email consistency: high

 
 
 
 
 
 
 

Affiliations

  • Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA. 2003 - 2004
  • Cardiovascular Division, Department of Medicine, Beth Israel Deaconess Medical Center, 330 Brookline Ave, USA. 2004

References

  1. 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) [Pubmed]
  2. 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) [Pubmed]
  3. 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) [Pubmed]
  4. 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) [Pubmed]
 
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