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Direct inhibition of c-Jun N-terminal kinase in sympathetic neurones prevents c-jun promoter activation and NGF withdrawal-induced death by Andreas Eilers; Jonathan Whitfield; Bina Shah; Cesare Spadoni; Howard Desmond; Jonathan Ham is a Neuroscience article available to read on EtoBox.

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c‐Jun N‐terminal kinases (JNKs) regulate gene expression by phosphorylating transcription factors, such as c‐Jun. Studies with __Jnk__ knockout mice suggest that JNK activity may be required for excitotoxin‐induced apoptosis in the adult hippocampus and for apoptosis in the developing embryonic neural tube. Here we investigate the role of JNKs in classical neurotrophin‐regulated developmental neuronal death by using nerve growth factor (NGF)‐dependent sympathetic neurones. In this system, NGF withdrawal leads to an increase in JNK activity, an increase in c‐Jun protein levels and c‐Jun N‐terminal phosphorylation before the cell death commitment point, and c‐Jun activity is required for cell death. To inhibit JNK activity in sympathetic neurones we have used two different JNK inhibitors that act by distinct mechanisms: the compound SB 203580 and the JNK binding domain (JBD) of JNK interacting protein 1 (JIP‐1). We demonstrate that JNK activity is required for c‐Jun phosphorylation, __c‐jun__ promoter activation and NGF withdrawal‐induced apoptosis. We also show that ATF‐2, a c‐Jun dimerization partner that can regulate __c‐jun__ gene expression, is activated following NGF deprivatio

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Author

Andreas Eilers; Jonathan Whitfield; Bina Shah; Cesare Spadoni; Howard Desmond; Jonathan Ham

Publisher

John Wiley and Sons; Wiley (Blackwell Publishing); Blackwell Publishing Inc.; Wiley (ISSN 0022-3042)

Published

2001

Language

EN

Field

Neuroscience (Life Sciences)