Figure 1. Ran/Crm1 functions as a loading dock to coordinate “licensing factors” that regulate centrosome duplication. The small GTPase, Ran, switches between an inactive GDP and an active GTP-bound state through interaction with RanBP1 and RCC1, respectively. During early G1 or mitosis, nucleophosmin (NPM) associates with centrosomes through its nuclear export signal (NES) interaction with the Ran/Crm1 complex, thus preventing centrosome reduplication. NPM is then phosphorylated and dissociates from the G1 centrosome upon activation of CDK2/cyclin E, or other kinases, to initiate centrosome duplication. NPM reassociates with mitotic centrosomes upon dephosphorylation. Thus, the Ran/Crm1 network serves as a loading lock to spatially and temporally coordinate NES-containing “licensing factors” that ensure the fidelity of the centrosome duplication process.