Modeling NDD-Associated NLGN2 Depletion Using CRISPR/Cas13 Reveals Exaggerated Process Elongation Mediated by the CCDC88A-G Protein–ELMO Axis
This work investigated the molecular basis of excessive neuronal process formation induced by depletion of NLGN2 using the N1E-115 cell line, an established model of neuronal differentiation, and identified the CCDC88A-G protein-ELMO signaling pathway as a key mediator of excessive neuronal morphogenesis following NLGN2 knockdown.