title: DAPK1 Signaling Pathways in Stroke: from Mechanisms to Therapies.
abstract: 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.
authors.affiliation: Department of Biotherapy Technology Center, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, 510120, China.
authors.forename: Shan
authors.initials: S
authors.lastname: Wang
authors.affiliation: Department of Biliary Pancreatic Surgery, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, 510120, China.
authors.forename: Xiangde
authors.initials: X
authors.lastname: Shi
authors.affiliation: Department of Physiology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.|The Institute for Brain Research (IBR), Collaborative Innovation Center for Brain Science, Huazhong University of Science and Technology, Wuhan, 430030, China.
authors.forename: Hao
authors.initials: H
authors.lastname: Li
authors.affiliation: Department of Physiology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.|The Institute for Brain Research (IBR), Collaborative Innovation Center for Brain Science, Huazhong University of Science and Technology, Wuhan, 430030, China.
authors.forename: Pei
authors.initials: P
authors.lastname: Pang
authors.affiliation: The Institute for Brain Research (IBR), Collaborative Innovation Center for Brain Science, Huazhong University of Science and Technology, Wuhan, 430030, China.|Department of Neurobiology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
authors.forename: Lei
authors.initials: L
authors.lastname: Pei
authors.affiliation: Department of Orthopedics, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, 510120, China. shenhuiyong@aliyun.com.
authors.forename: Huiyong
authors.initials: H
authors.lastname: Shen
authors.affiliation: Department of Physiology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China. lym@hust.edu.cn.|The Institute for Brain Research (IBR), Collaborative Innovation Center for Brain Science, Huazhong University of Science and Technology, Wuhan, 430030, China. lym@hust.edu.cn.
authors.forename: Youming
authors.initials: Y
authors.lastname: Lu
mesh_terms: D000818:Animals; D002545:Brain Ischemia / Q000201:enzymology / Q000473:pathology; D016923:Cell Death; D064550:Death-Associated Protein Kinases / Q000378:metabolism*; D006801:Humans; D009474:Neurons / Q000201:enzymology* / Q000473:pathology*; D015398:Signal Transduction; D020521:Stroke / Q000201:enzymology* / Q000628:therapy*
chemical_list: D064550:Death-Associated Protein Kinases
keywords: Cell death; DAPK1; Mechanism; Stroke; Therapeutics