T
Thomas D. Gilmore
Researcher at Boston University
Publications - 152
Citations - 12712
Thomas D. Gilmore is an academic researcher from Boston University. The author has contributed to research in topics: Transcription factor & REL. The author has an hindex of 51, co-authored 146 publications receiving 11962 citations. Previous affiliations of Thomas D. Gilmore include Harvard University & University of Wisconsin-Madison.
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Introduction to NF-kappaB: players, pathways, perspectives.
TL;DR: An overview of the discovery and current status of NF-κB as a research topic is provided and the organization and focus of articles included in the following reviews are described, as well as likely future areas of research interest on NF-σB.
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Control of apoptosis by Rel/NF-kappaB transcription factors.
TL;DR: An understanding of the role of Rel/NF-κB transcription factors in controlling apoptosis may lead to the development of therapeutics for a wide variety of human diseases, including neurodegenerative and immune diseases, and cancer.
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Inhibitors of NF-kappaB signaling: 785 and counting.
TL;DR: Over 750 inhibitors of the NF-κB pathway have been identified, including a variety of natural and synthetic molecules, which include antioxidants, peptides, small RNA/DNA, microbial and viral proteins, small molecules, and engineered dominant-negative or constitutively active polypeptides.
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Mutations in the NF-kappaB signaling pathway: implications for human disease.
G Courtois,Thomas D. Gilmore +1 more
TL;DR: This review describes human diseases in which mutations in the components of the core NF-κB signaling pathway have been implicated and discusses the molecular mechanisms by which these alterations in NF-σB signaling are likely to contribute to the disease pathology.
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Good cop, bad cop: the different faces of NF-κB
TL;DR: This review will discuss the different functions of NF-κB, the pathways that modulate NF- κB subunit activity and, in contrast to its more commonly thought of role as a promoter of cancer cell growth and survival, the ability of NF, under some circumstances, to behave as a tumor suppressor.