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.

Class 1 histone deacetylase (HDAC) inhibitor MS-275 enhances the efficacy of glucagon-like peptide 1 receptor (GLP-1R) therapy for glycemic control and reduction of obesity.

Exploiting virus-encoded ion channels as drug targets drove a multi-faceted approach to deriving potent small molecules targeting HCV p7, simultaneously providing new insights into its fundamental biology.

Plasmodium falciparum invasion protein EBA-175, once shed from the parasite surface post invasion, facilitates RBC clustering and enhances parasite growth while simultaneously enabling parasite immune evasion of host neutralizing antibodies.

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.

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.

Transport of double-stranded RNA from parental circulation to progeny using the transmembrane protein SID-1 can occur through multiple routes during C. elegans development and buffer heritable changes in gene expression.

Three-dimensional electron microscopy (3DEM) demonstrates the dependence on presynaptic mitochondria for vesicle mobilization as dendritic spines are silently added at P15 or synapses are silently enlarged in adults after long-term potentiation.