NDLI: A critical role of neural-specific JNK3 for ischemic apoptosis.

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A critical role of neural-specific JNK3 for ischemic apoptosis.

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A critical role of neural-specific JNK3 for ischemic apoptosis.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Davis, Roger J. Kuan, Chia-yi Flavell, Richard A. Rakic, Pasko Bao, Jue Schloemer, Aryn J. Whitmarsh, Alan J. Liao, Guanghong Yang, Derek D. Haddad, Gabriel G. Dong, Chen Banasiak, Kenneth J.
Description	Author Affiliation: Kuan CY ( Department of Pediatrics, Division of Developmental Biology, Children's Hospital Medical Center, Cincinnati, OH 45229, USA. alex.kuan@chmcc.org);
Abstract	c-Jun N-terminal kinase (JNK) signaling is an important contributor to stress-induced apoptosis, but it is unclear whether JNK and its isoforms (JNK1, JNK2, and JNK3) have distinct roles in cerebral ischemia. Here we show that JNK1 is the major isoform responsible for the high level of basal JNK activity in the brain. In contrast, targeted deletion of Jnk3 not only reduces the stress-induced JNK activity, but also protects mice from brain injury after cerebral ischemia-hypoxia. The downstream mechanism of JNK3-mediated apoptosis may include the induction of Bim and Fas and the mitochondrial release of cytochrome c. These results suggest that JNK3 is a potential target for neuroprotection therapies in stroke.
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	25
Volume Number	100
Language	English
Publisher	National Academy of Sciences
Publisher Date	2003-12-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Apoptosis Ischemia Mitogen-Activated Protein Kinases Physiology Protein-Tyrosine Kinases Animals Brain Metabolism Pathology Cells, Cultured Cytochromes c Enzyme Activation Glucose Hippocampus Anoxia Immunohistochemistry In Situ Nick-End Labeling Mice Mitochondria Mitogen-Activated Protein Kinase 10 Myocardium Cytology Neurons Oxygen Protein Isoforms RNA, Messenger Reverse Transcriptase Polymerase Chain Reaction Signal Transduction Time Factors Transcription, Genetic Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S. Multidisciplinary
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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