WT MRC Stem Cell Institute and Cambridge Centre for Brain Repair
Ischemic stroke continues to be a leading cause of morbidity/mortality throughout the world. The paucity of therapeutic options stands in stark contrast to the intensity of research efforts/number of clinical trials that have been performed. While reductionist methods have done much to enhance our understanding of ischemic brain injury, accumulating evidence has come to suggest that beyond the restoration of perfusion it will likely not be possible to identify a single dominant therapeutic target. Therefore, a focus on i) plurifunctional molecular pathways and ii) plurifunctional therapeutic modalities capable of influencing brain ischemia are urgently warranted. Critically, upregulation of the post-translational modification of proteins by the Small Ubiquitin-like MOdifier (SUMO) protein(s) via a process dubbed SUMOylation has been shown capable of maintaining homeostasis in natural models (e.g. hibernation) and in preclinical models of brain ischemia.
Magnetic resonance imaging (MRI)
Recombinant protein expression
Associated News Items
Bernstock JD, Lee YJ, Peruzzotti-Jametti L, Southall N, Johnson KR, Maric D, Volpe G, Kouznetsova J, Zheng W, Pluchino S, Hallenbeck JM. (2015), “A novel quantitative high-throughput screen identifies drugs that both activate SUMO conjugation via the inhibition of microRNAs 182 and 183 and facilitate neuroprotection in a model of oxygen and glucose deprivation.” J Cereb Blood Flow Metab.