Faculty Profiles

Thomas Gilmore

Thomas Gilmore

Professor of Biology

PhD, University of California, Berkeley, 1984
Areas of interest: molecular biology, cell biology, signal transduction, cancer, molecular ecology
gilmore@bu.edu
(617) 353-5444
http://www.nf-kb.org

Current Research

Much of our research focuses on three projects centered around transcription factor NF-kB.  In one project, we seek to understand the cellular and molecular mechanisms by which altered NF-kB activity contributes to a variety of human cancers, especially lymphoid cell cancers. For example, we have found that the human REL gene, which encodes an NF-kB transcription factor, is amplified and overexpressed in many human lymphomas and can also malignantly transform avian and human lymphoid cells in tissue culture. More recently, we have also been investigating the role of NF-kB co-activator proteins called HATs (histone acectyltransferases) in human B-cell lymphoma.

In collaborative studies with Drs. John Porco and Adrian Whitty in the Chemistry Department at Boston University, we are characterizing natural and synthetic inhibitors of NF-kB signaling. Many of these inhibitors are derivatives of natural products, and may have anti-cancer or anti-inflammatory activities.

Finally, we are studying the evolutionary origins of the NF-kB pathway by characterizing NF-kB genes and proteins in simple marine organisms, such as the sea anemone Nematostella vectensis. This research may have relevance to the mechanisms by which simple marine organisms deal with the environmental stress that is currently impacting sensitive marine ecosystems. These studies are being carried out in collaboration with Drs. Les Kaufman, John Finnerty and Trevor Siggers (Biology Department, Boston University).

Courses Taught

  • BB522 Molecular Biology Laboratory
  • BI576 Carcinogenesis

Selected Publications

  • Haery L, Lugo-Pico JG, Henry RA, Andrews AW, Gilmore TD (2014) Histone acetyltransferase-deficient p300 mutants in diffuse large B-cell lymphoma have altered transcriptional regulatory activities and are required for optimal cell growth. Molecular Cancer 13: 29
  • Cote SM, Gilmore TD, Shaffer R, Weber U, Bollam R, Golden MS, Glover K, Herscovitch M, Ennis T, Allen KN, Whitty A (2013) Mutation of nonessential cysteines shows that the NF-kB essential modulator (NEMO) forms a constitutive noncovalent dimer that binds IkB kinase-beta with high affinity. Biochemistry, 52:9141-9154.
  • Wolenski FS, Layden MJ, Martindale MQ, Gilmore TD, Finnerty JR (2013) Characterizing the spatiotemporal expression of RNAs and proteins in the starlet sea anemone, Nematostella vectensis. Nature Protocols, 8: 900-915.
  • Thompson RC, Vardinogiannis I, Gilmore TD. (2013) The sensitivity of diffuse large B-cell lymphoma cell lines to histone deacetylase inhibitor-induced apoptosis is modulated by BCL-2 family protein activity. PLoS ONE, 8: e62822.
  • Wolenski FS, Bradham CA, Finnerty JR, Gilmore TD(2013) NF-kB is required for cnidocyte development in the sea anemone Nematostella vectensis. Developmental Biology, 373: 205-215.
  • Gilmore TD, Wolenski FS (2012) NF-kB: where did it come from and why? Immunological Reviews, 246: 14-25.
  • Wolenski FS, Chandani S, Stefanik DJ, Jiang N, Chu E, Finnerty JR, Gilmore TD (2011) Two polymorphic residues account for the differences in DNA binding and transcriptional activation by NF-kB proteins encoded by naturally occurring alleles in Nematostella vectensis. Journal of Molecular Evolution, 73: 325-336.
  • Gilmore TD, Gerondakis S (2011) The c-Rel transcription factor in development and disease. Genes & Cancer 7, 695-711.

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