Stephen Tait
Reader
Deprtment of Oncology
University of Glasgow
United Kingdom
Biography
Dr Stephen Tait is currently working as a Reader (Beatson Institute for Cancer Research)
Research Interest
Mitochondria and Cell Death: Cell death is a key tumour suppressor mechanism that must be inhibited in order for cancer to develop. Sensitivity to cell death also governs therapeutic efficacy because anti-cancer therapies often act by killing cells. The major form of programmed cell death is apoptosis, a process in which mitochondria play an essential role. Our research focuses upon understanding how mitochondria control cell death and addressing how this is deregulated in cancer. Clinical translation of our findings should lead to improvements of existing therapies and development of new approaches to enable tumour selective killing.
Publications
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Ichim, G. and Tait, S. W.G. (2017) Cancer therapy-induced PAFR ligand expression: any role for caspase activity? Nature Reviews Cancer, 17(4), p. 253. (doi:10.1038/nrc.2017.16) (PMID:28280269)
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Daniels, B. P., Snyder, A. G., Olsen, T. M., Orozco, S., Oguin III, T. H., Tait, S. W.G., Martinez, J., Gale, M., Loo, Y.-M. and Oberst, A. (2017) RIPK3 restricts viral pathogenesis via cell death-independent neuroinflammation. Cell, 169(2), 301-313.e11. (doi:10.1016/j.cell.2017.03.011) (PMID:28366204)
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Giampazolias, E. et al. (2017) Mitochondrial permeabilization engages NF-κB-dependent anti-tumour activity under caspase deficiency. Nature Cell Biology, 19(9), pp. 1116-1129. (doi:10.1038/ncb3596) (PMID:28846096)
