A critical role of neural-specific JNK3 for ischemic apoptosis

Chia Yi Kuan, Alan J. Whitmarsh, Derek D. Yang, Guanghong Liao, Aryn J. Schloemer, Chen Dong, Jue Bao, Kenneth J. Banasiak, Gabriel G. Haddad, Richard A. Flavell, Roger J. Davis, Pasko Rakic

    Research output: Contribution to journalArticlepeer-review


    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.
    Original languageEnglish
    Pages (from-to)15184-15189
    Number of pages5
    JournalProceedings of the National Academy of Sciences of the United States of America
    Issue number25
    Publication statusPublished - 9 Dec 2003


    Dive into the research topics of 'A critical role of neural-specific JNK3 for ischemic apoptosis'. Together they form a unique fingerprint.

    Cite this