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Shigeki Miyamoto, Ph.D.

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Miyamoto photo Professor of Oncology

B.A., 1985, Biochemistry/Molecular Biology, University of California-Santa Cruz
Ph.D., 1990, Cancer Research/Endocrinology, University of California-Berkeley
Postdoctoral research: Salk Institute, San Diego

Office: 6159 Wisconsin Institutes for Medical Research (WIMR)
Telephone: Office - (608) 262-9281; Lab - (608) 265-8595
Email: smiyamot@wisc.edu

Lab Home Page

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Research Interests: Regulation of the transcription factor NF-κB as a model system to study cancer

Research Description: Over the last two decades, the Miyamoto lab has pursued a variety of research interests centered around cell signaling and asked "what happens when cells are no longer able to communicate effectively?" Most of the current research is focused on understanding the NF-κB signaling pathway as a model. Our lab, and others, have shown that NF-κB is key in promoting cell survival (anti-apoptotic), normal immune system development, stress response, early embryonic development, cell adhesion, and tumor metastasis.

With regard to the NF-κB model, our lab has two overarching research interests. First, we are interested in characterizing how nuclear stress conditions, such as DNA damage, induce signaling events in the cytoplasm. Second, we are interested in how cancer cells use signaling mechanisms for their growth and survival advantages to evade anticancer drug effects.  We are currently focusing on the NF-κB signaling system as an important paradigm to increase our understanding of these processes.

Selected publications

Hebron, E., Hope, C., Kim, J., Jensen, J. L., Flanagan, C., Bhatia, N., Maroulakou, I., Mitsiades, C., Miyamoto, S., Callander, N., Hematti, P., and Asimakopoulos, F.  MAP3K8 Kinase Regulates Myeloma Growth by Cell-Autonomous and Non-Autonomous Mechanisms Involving Myeloma-Associated Monocytes/Macrophages.  Brit. J. Haematol., 160(6): 779-784, 2013.

McCool, K. W., and Miyamoto, S.  DNA Damage-Dependent NF-κB Activation:  NEMO Turns Nuclear Signaling Inside Out.  Immunol. Rev., 246:  311-326, 2012.

Young, E. W. K., Pak, C., Kahl, B. S., Yang, D. T., Callander, N. S., Miyamoto, S., and Beebe, D. J.  Microscale Functional Cytomics for Studying Hematologic Cancers.  Blood, 119: e76-e85, 2012.

Lee, M.-H., and Miyamoto, S.  Expanding NFκB and SUMO Ties.  Cell Cycle, 10:  3983-3984, 2011.

Lee, M. H., Mabb, A. M., Gill, G. B., Yeh, E. T. H., and Miyamoto, S.  NF-κB Induction of the SUMO Protease SENP2:  A Negative Feedback Loop to Attenuate Cell Survival Response to Genotoxic Stress.  Mol. Cell, 43:  180-191, 2011.

Martin, S. E., Wu, Z.-H., Gehlhaus, K., Jones, T. L., Zhang, Y.-W., Guha, R., Miyamoto, S., Pommier, Y., and Caplen, N. J.  RNAi Screening Identifies TAK1 as a Potential Target for the Enhanced Efficacy of Topoisomerase Inhibitors.  Curr. Cancer Drug Targets, 11:  976-986, 2011.

Miyamoto, S.  Nuclear Initiated NF-κB Signaling:  NEMO and ATM Take Center Stage.  Cell Res., 21:  116-130, 2011.

Wu, L., Shao, L., An, N., Wang, J., Pazhanisamy, S., Feng, W., Hauer-Jensen, M., Miyamoto, S., and Zhou, D.  IKKβ Regulates the Repair of DNA Double-Strand Breaks Induced by Ionizing Radiation in MCF-7 Breast Cancer Cells.  PLoS One, 6(4):e18447, 2011.

Wuerzberger-Davis, S. M., Chen, Y., Yang, D. T., Kearns, J. D., Bates, P. W., Lynch, C., Ladell, N. C., Yu, M., Podd, A., Zeng, H., Huang, T. T., Wen, R., Hoffmann, A., Wang, D., and Miyamoto, S.  Nuclear Export of the NF-κB Inhibitor IκBα Is Required for Proper B Cell and Secondary Lymphoid Tissue Formation.  Immunity, 34: 188-200, 2011.

Yang, Y., Xia, F., Hermance, N., Mabb, A., Simonson, S., Morrissey, S., Gandhi, P., Munson, M., Miyamoto, S., and Kelliher, M. A.  A Cytosolic ATM/NEMO/RIP1 Complex Recruits TAK1 To Mediate the NF-κB and p38 Mitogen-Activated Protein Kinase (MAPK)/MAPK-Activated Protein 2 Responses to DNA Damage.  Mol. Cell. Biol., 31:  2774-2786, 2011.

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