The c-Jun transcription factor – bipotential mediator of neuronal death, survival and regeneration

Axon interruption elicits a complex neuronal response that leaves neurons poised precariously between death and regeneration

Thomas Herdegen

2002

Scholarcy highlights

  • Axon interruption elicits a complex neuronal response that leaves neurons poised precariously between death and regeneration
  • The transcription factor c-Jun is one of the earliest and most consistent markers for neurons that respond to nerve-fiber transection, and its expression can be related to both degeneration and survival including target re-innervation
  • In vitro experiments have demonstrated that expression of c-Jun can kill neonatal neurons but, in the adult nervous system, c-Jun might be involved in neuroprotection and regeneration
  • The functional characteristics of c-Jun offer a model for the ability of a single molecule to serve as pivotal regulator for death or survival, in the response of the cell body to axonal lesions and following neurodegenerative disorders
  • The fate of neurons is determined by a novel transcriptional network comprising c-Jun, ATF-2 and JNKs
  • We recommend that commenters identify themselves with full names and affiliations

Need more features? Save interactive summary cards to your Scholarcy Library.