The p75 neurotrophin receptor prevents the migration of the granule cell precursors away from its mitogenic niche in the external granule layer of the cerebellum, by maintaining a pool of undifferentiated cells capable of responding to mitogenic signals.

A novel neurotrophin signaling axis underpins a behavioral response to food scarcity.

The hair follicle dermal condensate is populated via migration, and the cells exhibit early changes in cell shape and cell cycle status; Fgf20 primes these cellular and molecular events.

Structures of the death domain of the p75 neurotrophin receptor in complex with downstream effectors show how competitive protein-protein interactions orchestrate the hierarchical activation of downstream pathways in non-catalytic receptors.

Induction of the fission of mitochondria-populating sensory axons is shown to be a novel biological action of neurotrophins.

A distinct subset of cerebellar nuclei neurons originates from a previously unrecognized germinal zone within the cerebellar primordium, independent of Atoh1 influence, highlighting new cellular origins in cerebellar development.

In mouse models of Huntington's disease, striatal spiny projection neurons up-regulate dendritic potassium channels, which impairs their normal function, but a zinc finger gene therapy can reverse this deficit.

The nerve growth factor receptor (NGFR) protein regulates p53 via two negative feedback mechanisms, which are hijacked by cancer cells.

In vivo experiments on transgenic mice, and cell culture studies, establish Schwann cell c-Jun as a central regulator of peripheral nerve repair, and repair failure, during aging and chronic denervation.

BDNF axonal signaling regulates protein synthesis in neuronal cell bodies leading to dendritic arborization through dynein-dependent transport of signaling endosomes.