Loss of SEZ6L2 disrupts synaptic architecture and drives progressive behavioral deficits
Julia M. Granato, Nina Silver, Alison Hobbins, John Randolph, Angela Stout, Harris A. Gelbard, Jenny M Gunnersen, Samuel Mackenzie, Patricia M. White, Jennetta W. Hammond
This study characterizes Sez6l2 knockout mice, showing behavioral and synaptic deficits, and compares them to Sez6 triple knockout mice, highlighting SEZ6L2's non-redundant role in brain function.
bioRxiv · Sep 24, 2026 · PreprintNeuroscience