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

指紋

Glycolysis
Cytomegalovirus
Mitochondria
Mitochondrial Degradation
Apoptosis
Mitochondrial Turnover
Phosphofructokinases
Mitochondrial Diseases
Oxidopamine
Oxidative Phosphorylation
Parkinson Disease
Proteins
Oxidative Stress
Cell Death
Calcium
Neuroprotection
cytomegalovirus IE1 protein

ASJC Scopus subject areas

  • General

引用此文

The Cytomegalovirus protein pUL37×1 targets mitochondria to mediate neuroprotection. / Hong, Chien Tai; Chau, Kai Yin; Schapira, Anthony H V.

於: Scientific Reports, 卷 6, 31373, 26.08.2016.

研究成果: 雜誌貢獻文章

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