A critical role of neural-specific JNK3 for ischemic apoptosis
AUTOR(ES)
Kuan, Chia-Yi
FONTE
National Academy of Sciences
RESUMO
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.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=299947Documentos Relacionados
- Mammalian Scratch: A neural-specific Snail family transcriptional repressor
- n-Sec1: a neural-specific syntaxin-binding protein.
- CoREST: A functional corepressor required for regulation of neural-specific gene expression
- Identification of a neural-specific cDNA, NPDC-1, able to down-regulate cell proliferation and to suppress transformation.
- A single zinc finger motif in the silencing factor REST represses the neural-specific type II sodium channel promoter