期刊
MOLECULAR NEUROBIOLOGY
卷 54, 期 6, 页码 4716-4722出版社
SPRINGER
DOI: 10.1007/s12035-016-0008-y
关键词
DAPK1; Stroke; Cell death; Mechanism; Therapeutics
资金
- National Natural Science Foundation of China [81130079, 91232302]
- Key Project of United Fund of National Natural and Guangdong Province [U1301223]
- Medical Scientific Research Foundation of Guangdong Province, China [A2016304]
Death-associated protein kinase 1 (DAPK1), a Ca2+/calmodulin (CaM)-dependent serine/threonine protein kinase, plays important roles in diverse apoptosis pathways not only in tumor suppression but also in neuronal cell death. The requirement of DAPK1 catalytic activity for its proposed cell functions and the elevation of catalytic activity of DAPK1 in injured neurons in models of neurological diseases, such as ischemia and epilepsy, validate that DAPK1 can be taken as a potential therapeutic target in these diseases. Recent studies show that DAPK1-NR2B, DAPK1-DANGER, DAPK1-p53, and DAPK1-Tau are currently known pathways in stroke-induced cell death, and blocking these cascades in an acute treatment effectively reduces neuronal loss. In this review, we focus on the role of DAPK1 in neuronal cell death after stroke. We hope to provide exhaustive summaries of relevant studies on DAPK1 signals involved in stroke damage. Therefore, disrupting DAPK1-relevant cell death pathway could be considered as a promising therapeutic approach in stroke.
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