Background: Cell stress and tissue injury lead to c-Jun N-terminal kinase (JNK) activation, which is known to contribute to cell death. Paradoxically, strong evidence supports an important role for JNK in the regeneration of neuronal processes, subsequent to injury.
Objective: Recent research revealed the growth cone-associated protein superior cervical ganglion-10 protein as a candidate effector for the regeneration pathway mediated by JNK1. This implies that neuroprotective strategies targeting JNK may have negative effects on neuronal regeneration, unless JNK1 function is spared, and that the mechanistic relationships between JNK1 and neuronal regeneration deserve increased attention.
Results: This review proposes a model reconciling the microtubule regulatory properties of superior cervical ganglion protein 10 with its role as a JNK effector of regeneration and highlight remaining issues to be resolved.