The Cytomegalovirus protein pUL37×1 targets mitochondria to mediate neuroprotection

Chien Tai Hong, Kai Yin Chau, Anthony H V Schapira

研究成果: 雜誌貢獻文章

摘要

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.
原文英語
文章編號31373
期刊Scientific Reports
6
DOIs
出版狀態已發佈 - 八月 26 2016

ASJC Scopus subject areas

  • General

指紋 深入研究「The Cytomegalovirus protein pUL37×1 targets mitochondria to mediate neuroprotection」主題。共同形成了獨特的指紋。

  • 引用此