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Sci Rep. 2016 Aug 26;6:31373. doi: 10.1038/srep31373.

The Cytomegalovirus protein pUL37×1 targets mitochondria to mediate neuroprotection.

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Department of Clinical Neuroscience, UCL Institute of Neurology, University College London, UK.
Department of Neurology, Shuang Ho Hospital, Taipei Medical University, New Taipei City, Taiwan.
Department of Neurology, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan.


There is substantial evidence that mitochondrial dysfunction plays a significant role in the pathogenesis of Parkinson disease (PD). This contribution probably encompasses defects of oxidative phosphorylation, mitochondrial turnover (mitophagy), mitochondrial derived oxidative stress, and apoptotic signalling. Human cytomegalovirus immediate-early protein pUL37 × 1 induces Bax mitochondrial translocation and inactivation to prevent apoptosis. Over-expressing pUL37 × 1 in neuronal cells protects against staurosporin and 6-hydroxydopamine induced apoptosis and cell death. Protection is not enhanced by bax silencing in pUL37 × 1 over-expressing cells, suggesting a bax-dependent mechanism of action. pUL37 × 1 increases glycolysis and induces mitochondrial hyperpolarization, a bax independent anti-apoptotic action. pUL37 × 1 increases glycolysis through activation of phosphofructokinase by a calcium-dependent pathway. The dual anti-apoptotic mechanism of pUL37 × 1 may be considered a novel neuroprotective strategy in diseases where mitochondrial dysfunction and apoptotic pathways are involved.

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