Alternative splicing of the Dcc gene, which is controlled by the NOVA RNA-binding proteins, is crucial during neuronal migration and axon guidance.

Mathematical modelling explains why molecular gradients sometimes cause axons to only turn weakly.

The Roundabout2 receptor acts non-autonomously to promote commissural axons to cross the midline by antagonizing Slit-dependent axon repulsion.

Mature axons lose the ability to regenerate because key growth molecules are excluded through changes in vesicle transport, and restoring transport can restore regeneration.

EphA signaling plays dual opposite roles on axon dynamics in neurons, so it inhibits and promotes axon growth through ligand binding and receptor processing, respectively.

A novel ALS-associated variant in UBQLN4 impairs proteasome function and beta-catenin degradation to drive aberrant axon morphogenesis in motor neurons.

The kinase AKT acts as a nodal point that coordinates both positive and negative cues to regulate the regeneration of central nervous system axons in adult mice.

Genetic study of C. elegans neural development reveals the function of glia-neuron gap junctions in neuronal axon specification, and shows that glial cells regulate neuronal intracellular pathways through gap junctions.

In C. elegans and mouse neurons, the balance between poly(ADP-ribose) glycohydrolases and poly(ADP-ribose) polymerases regulates axon regeneration downstream of DLK-1/MAPKKK signaling.

The AKT-GSK3β-eIF2Bε signaling module plays a key role in promoting axon regeneration in the adult mammalian central nervous system.