The p85α homodimer plays a role in the PI3K pathway by regulating PTEN function.

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.

The p75 neurotrophin receptor regulates when granule neuron progenitors exit the cell cycle in the developing cerebellum.

Vangl2 induced by inflammation recruits ubiquitin ligase PDLIM2 and increases K63-linked ubiquitination on p65, which promotes the recognition of p65 by cargo receptor NDP52 and the autophagic degradation of p65.

OPC-specific genetic inhibition of Akt upstream and downstream molecules in the mouse, and simultaneous OPC fate analysis reveal that PTEN-AKT-GSK3b forms a persistent negative signaling pathway for OL development, in parallel with the AKT-mTORC1 pathway.

Cells of the mammalian cochlea can be reprogrammed to produce mechanosensory hair cells, but epigenetic changes in the cochlea make this process less efficient with age.

Linker histones affect the lineage determination of granulocyte precursor cells via regulation of the transcription factor GATA-2.

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

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.