Model of tripartite protein-protein interactions between Cend1, RanBPM, and Dyrk1B regulating NPC cell cycle progression/exit and neuronal differentiation. In NPCs, where expression of Cend1 is low, RanBPM binds Dyrk1B in the nucleus and facilitates its degradation by the 26S proteasome. Thus, Cyclin D1 remains active in the nucleus to drive cell cycle progression. Before terminal mitosis of NPCs, Cend1 expression rises and stays high in postmitotic neurons where it binds to and restrains RanBPM to the cytoplasm. Consequently, Dyrk1B kinase is maintained intact in the nucleus, where it signals cell cycle exit by phosphorylation of Cyclin D1 resulting in its degradation.