Gail E. Sonenshein, Ph.D.

Professor, Department of Biochemistry
Director, Program in Research on Women’s Health

B.S.      Brooklyn Polytechnic Institute
PH.D.  Massachusetts Institute of Technology

soneshein3

Major interests of my laboratory center on the Rel/NF-kappaB family of transcription factors and on the c-myc oncogene, which play pivotal roles in the control of cell proliferation, apoptosis and neoplastic transformation. Research efforts are divided into two projects: 1) Rel/NF-kappaB family activity. This lab has made several key discoveries on the roles of the Rel family of transcription factors. Rel factors were shown to regulate c-myc gene transcription, through two functional elements. Furthermore, Rel factors were found to protect various cancer cells from apoptosis, including B cell lymphomas and breast cancer cells. Studies are in progress to characterize the mechanism by which various agents affect Rel family activity, such as anti-Ig treatment, CD40L, and TGF-beta 1. 2) c-Myc function. The c-Myc protein is believed to function both as a transcriptional activator, as well as a repressor. Max protein has been shown to play a central role facilitating c-Myc binding to an E-box, promoting its ability to transactivate. A naturally occurring variant form of Max (termed dMax), missing the basic region and first helix and loop, has been identified and shown to selectively down-regulate c-Myc activator ability, in a dominant fashion. Lastly, a novel mechanism whereby c-Myc inhibits transcription of genes that contain an initiator (Inr) element has been discovered. Experiments to further elucidate this mechanism are in progress.

Representative Publications:

  1. Wu, M., H. Lee, R.E. Bellas, S.L. Schauer, M. Arsura, D. Katz, M. FitzGerald, T.L. Rothstein, D.H. Sherr and G.E. Sonenshein. 1996. Inhibition of NF-kappaB/Rel induces apoptosis of murine B cells. EMBO J. 15:4682-4690.
  2. Pianetti, S., M.Arsura, R.Romieu-Mourez, R.J. Coffey, and G.E. Sonenshein. 2001. Her-2/neu overexpression induces NF-kappaB via a PI3-kinase/Akt pathway without IKK activation that can be inhibited by the tumor suppressor PTEN. Oncogene 20: 1287-1299.
  3. Yang, W., J.Shen, M.Wu, M.Arsura, M.Fitzgerald, Z.Suldan, D.W.Kim, C.S.Hofmann, S. Pianetti, R.Romieu-Mourez, L.P. Freedman and G.E. Sonenshein. 2001. Repression of transcription of the p27Kip1 cyclin-dependent kinase inhibitor gene by c-Myc. Oncogene 20: 1688-1702.
  4. Romieu-Mourez, R., E.Landesman-Bollag, D.C.Seldin, A.M.Traish, F.Mercurio, and G.E. Sonenshein. 2001. Roles of IKK kinases and protein kinase CK2 in activation of NF-kappaB in breast cancer. Cancer Res. 61: 3810-3818.
  5. Shen, J., P. Channavajhala, D.C. Seldin, and G.E. Sonenshein. 2001. Phosphorylation by the protein kinase CK2 promotes calpain-mediated degradation of Ikappa B alpha. J. Immunol 167:4919-4925.
  6. Jiang, H.Y., C. Petrovas, & G.E. Sonenshein. 2002. RelB/p50 NF-kappa B complexes are selectively induced by the cytomegalovirus IE1 protein: differential regulation of Bcl-xL promoter activity by NF-kappa B family members. J. Virol. 76:5737-5747.

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Primary teaching affiliate
of BU School of Medicine