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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Julie R. McMullen

Beth Israel Deaconess Medical Center

Harvard Medical School


MA 02215



Name/email consistency: high



  • 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


  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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