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Jeremy R. Graff

Lilly Research Labs

Eli Lilly and Company

Indianapolis

Indiana 46285

[email]@lilly.com

Name/email consistency: high

 
 
 
 
 
 
 

Affiliations

  • Lilly Research Labs, Eli Lilly and Company, Indianapolis, Indiana 46285. 2000 - 2010
  • Cancer Growth and Translational Genetics, Lilly Research Laboratories, Eli Lilly and Company, Indianapolis, USA. 2008
  • Comprehensive Cancer Center, Johns Hopkins University, Baltimore, Maryland 21231, USA. 2000

References

  1. Modulation of 4E-BP1 function as a critical determinant of enzastaurin-induced apoptosis. Dumstorf, C.A., Konicek, B.W., McNulty, A.M., Parsons, S.H., Furic, L., Sonenberg, N., Graff, J.R. Mol. Cancer Ther. (2010) [Pubmed]
  2. eIF4E activation is commonly elevated in advanced human prostate cancers and significantly related to reduced patient survival. Graff, J.R., Konicek, B.W., Lynch, R.L., Dumstorf, C.A., Dowless, M.S., McNulty, A.M., Parsons, S.H., Brail, L.H., Colligan, B.M., Koop, J.W., Hurst, B.M., Deddens, J.A., Neubauer, B.L., Stancato, L.F., Carter, H.W., Douglass, L.E., Carter, J.H. Cancer Res. (2009) [Pubmed]
  3. Targeting the eukaryotic translation initiation factor 4E for cancer therapy. Graff, J.R., Konicek, B.W., Carter, J.H., Marcusson, E.G. Cancer Res. (2008) [Pubmed]
  4. Therapeutic suppression of translation initiation factor eIF4E expression reduces tumor growth without toxicity. Graff, J.R., Konicek, B.W., Vincent, T.M., Lynch, R.L., Monteith, D., Weir, S.N., Schwier, P., Capen, A., Goode, R.L., Dowless, M.S., Chen, Y., Zhang, H., Sissons, S., Cox, K., McNulty, A.M., Parsons, S.H., Wang, T., Sams, L., Geeganage, S., Douglass, L.E., Neubauer, B.L., Dean, N.M., Blanchard, K., Shou, J., Stancato, L.F., Carter, J.H., Marcusson, E.G. J. Clin. Invest. (2007) [Pubmed]
  5. The protein kinase Cbeta-selective inhibitor, Enzastaurin (LY317615.HCl), suppresses signaling through the AKT pathway, induces apoptosis, and suppresses growth of human colon cancer and glioblastoma xenografts. Graff, J.R., McNulty, A.M., Hanna, K.R., Konicek, B.W., Lynch, R.L., Bailey, S.N., Banks, C., Capen, A., Goode, R., Lewis, J.E., Sams, L., Huss, K.L., Campbell, R.M., Iversen, P.W., Neubauer, B.L., Brown, T.J., Musib, L., Geeganage, S., Thornton, D. Cancer Res. (2005) [Pubmed]
  6. Emerging targets in the AKT pathway for treatment of androgen-independent prostatic adenocarcinoma. Graff, J.R. Expert Opin. Ther. Targets (2002) [Pubmed]
  7. Integrin-linked kinase expression increases with prostate tumor grade. Graff, J.R., Deddens, J.A., Konicek, B.W., Colligan, B.M., Hurst, B.M., Carter, H.W., Carter, J.H. Clin. Cancer Res. (2001) [Pubmed]
  8. Methylation patterns of the E-cadherin 5' CpG island are unstable and reflect the dynamic, heterogeneous loss of E-cadherin expression during metastatic progression. Graff, J.R., Gabrielson, E., Fujii, H., Baylin, S.B., Herman, J.G. J. Biol. Chem. (2000) [Pubmed]
  9. Increased AKT activity contributes to prostate cancer progression by dramatically accelerating prostate tumor growth and diminishing p27Kip1 expression. Graff, J.R., Konicek, B.W., McNulty, A.M., Wang, Z., Houck, K., Allen, S., Paul, J.D., Hbaiu, A., Goode, R.G., Sandusky, G.E., Vessella, R.L., Neubauer, B.L. J. Biol. Chem. (2000) [Pubmed]
 
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