The Notch signaling pathway can use its various ligands, receptors, and Fringe proteins to generate diverse intra- and intercellular signaling behaviors.

A new native prion protein aggregation assay shows that syntaxin-6, a risk factor for sporadic Creutzfeldt–Jakob disease, delays prion protein fibril formation and prolongs the presence of toxic aggregation intermediates.

The α1 isoform of synGAP restricts the binding of AMPA-receptors and other regulatory proteins to PSD-95, and thus regulates synaptic strength.

Syntaxin 4 regulates retrograde signaling in the postsynaptic compartment at Drosophila synapses by controlling trafficking of Neuroligin and Synaptotagmin 4 cargo.

Activation of Notch receptors by ligands in the same cell (cis-activation) is a prevalent and functional mode of signaling in the Notch pathway, and co-exists with trans-activation and cis-inhibition.

The autophagosomal membrane becomes negatively charged during maturation due to the accumulation of PI4P, leading to the recruitment of syntaxin 17, which is required for autophagosome-lysosome fusion.

Deletion of one copy of the postsynaptic density protein synGAP in rodents causes an increase in the level of the AMPA receptor auxiliary protein TARP in PSDs only in females.

A mutant rescue approach in STX1-null autaptic neurons provides definitive answers and opens up new questions into a controversial matter of syntaxin-1's binding to Munc18-1 through its N-peptide and its function in neurotransmission.

A cross-linking screen finds proteins that interact with TANGO1 to export Procollagen VII, and suggests a new model for the secretion of these bulky cargoes that are involved in skin and bone formation.

Detailed SYNGAP1 splice variant characterization uncovers distinct isoform functions and biochemical properties contributing to critical aspects of neurodevelopment, providing previously unknown isoform-level insight into SYNGAP1-related cognitive disorders.