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• W2020062883 abstract "c-Jun N-terminal kinase (JNK), along with its upstream activator MEKK-1, is typically thought of as a stress-activated kinase that mediates apoptosis. However, additional studies indicate that the MEKK-1/JNK pathway mediates critical aspects of neuronal survival and differentiation. Herein, we demonstrate that transfection of differentiated NB2a/d1 cells with a construct expression constitutively activated (ca) MEKK-1 increases levels of phospho-dependent neurofilament (NF) immunoreactivity within perikarya, while expression of a dominant-negative (dn) form of MEKK-1 decreases it. Steady-state levels of perikaryal phospho-NF immunoreactivity are reduced and the increase resulting from expression of caMEKK-1 is prevented, by the JNK inhibitor SP600125, suggesting that JNK is a major downstream effector of MEKK-1 on NF phosphorylation. Unexpectedly, both caMEKK-1 and dnMEKK-1 inhibited neuritogenesis as well as translocation of NFs into newly elaborated neurites. The JNK inhibitor SP600125 also inhibited NF transport in a dose-dependent manner. caMEKK-1 also prevented the increase in NF transport otherwise mediated by MAP kinase. Finally, both caMEKK-1 and dnMEKK-1 prevented initial neuritogenesis. These findings indicate that the MEKK-1/JNK pathway regulates critical aspects of initial outgrowth, and subsequent stabilization of axonal neurites." @default.
• W2020062883 created "2016-06-24" @default.
• W2020062883 creator A5059634441 @default.
• W2020062883 creator A5060354305 @default.
• W2020062883 creator A5091760549 @default.
• W2020062883 date "2006-12-01" @default.
• W2020062883 modified "2023-10-16" @default.
• W2020062883 title "Divergent effects of the MEKK-1/JNK pathway on NB2a/d1 differentiation: Some activity is required for outgrowth and stabilization of neurites but overactivation inhibits both phenomena" @default.
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• W2020062883 doi "https://doi.org/10.1016/j.brainres.2006.09.036" @default.
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