Exploring how UBQLN2 mutations cause ALS leads to the discovery of a pathway by which an ancient retroelement changes gene expression in human cells.

Axon guidance genes are conserved regulators of neurodegeneration in Drosophila melanogaster and human inducible motor neuron models of UBQLN2-associated amyotrophic lateral sclerosis.

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

Stimulation of cells with a mitochondria-depolarizing mitogen reveals a requirement for UBQLN1 expression in maintaining protein synthesis levels during cell cycle entry.

Maintenance of ubiquitin homeostasis is essential for proper control of the size of postsynaptic density and the growth of specialized membrane structure.

Interneuron-specific alternative splice variants of the synaptic receptor neurexin are critical for hippocampal network activity and short-term memory.

A genetic manipulation of the Nrxn1/3^SS4+-Cbln1/2 complex reveals this signaling pathway has no role in synapse formation but functions to shape the NMDAR- and AMPAR-content at multiple types of synapses with distinct facets in diverse circuits.

Pyramidal cells of the subiculum, a major output cell type of the hippocampus, can be deconstructed into distinct subtypes that exhibit a patchwork-like organization in space.

Impaired nuclear import of the transcription factor TFEB/MITF is a major cause of autophagy and lysosome dysfunction in amyotrophic lateral sclerosis caused by mutations in the C9orf72 gene.

A guide summarizing the diversity of cell types in the parabrachial nucleus.