T
Thomas G. Cotter
Researcher at University College Cork
Publications - 251
Citations - 20930
Thomas G. Cotter is an academic researcher from University College Cork. The author has contributed to research in topics: Apoptosis & Programmed cell death. The author has an hindex of 68, co-authored 251 publications receiving 19556 citations. Previous affiliations of Thomas G. Cotter include Tyndall National Institute & La Jolla Institute for Allergy and Immunology.
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ROS signalling in the biology of cancer.
TL;DR: The generation and sources of ROS within tumour cells, the regulation of ROS by antioxidant defence systems, as well as the effect of elevated ROS production on their signalling targets in cancer are discussed.
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Dose-dependent induction of apoptosis in human tumour cell lines by widely diverging stimuli
TL;DR: It is shown that cell death induced by a range of varied agents may take the form of either apoptosis or necrosis, and cells which are not killed directly, but merely injured by these agents, have the capacity to activate an internally programmed suicide death mechanism.
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Apoptosis and cancer: the genesis of a research field.
TL;DR: How the field of apoptosis biology has developed in the context of its contribution to the authors' understanding of cell death, or lack of it, in the development of malignant disease is focused on.
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Bax-induced Caspase Activation and Apoptosis via Cytochromec Release from Mitochondria Is Inhibitable by Bcl-xL
TL;DR: It would appear that the mitochondrial release of factors such as cytochrome c represents a critical step in committing a cell to death, and this release is independent of permeability transition and caspase activation but is inhibited by Bcl-xL.
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Role for c-myc in activation-induced apoptotic cell death in T cell hybridomas
Yufang Shi,Jacqueline M. Glynn,Lawrence J. Guilbert,Thomas G. Cotter,Reid P. Bissonnette,Douglas R. Green +5 more
TL;DR: Antisense oligonucleotides corresponding to c-myc block the constitutive expression of c-Myc protein in T cell hybridomas and interfere with all aspects of activation-induced apoptosis without affecting lymphokine production in these cells.