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pubmed-article:17379825pubmed:abstractTextDelayed neuronal death is a hallmark feature of stroke and the primary target of neuroprotective strategies. Caspase-independent apoptosis pathways are suggested as a mechanism for the delayed neuronal injury. Here we test the hypothesis that one of the caspase-independent apoptosis pathways is activated by BNIP3 and mediated by EndoG.lld:pubmed
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pubmed-article:17379825pubmed:articleTitleBNIP3 upregulation and EndoG translocation in delayed neuronal death in stroke and in hypoxia.lld:pubmed
pubmed-article:17379825pubmed:affiliationDepartment of Human Anatomy and Cell Science, University of Manitoba, Faculty of Medicine, Winnipeg, Manitoba, Canada.lld:pubmed
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