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. 2023 Jul 28;14:1215110. doi: 10.3389/fpsyt.2023.1215110

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Copyright © 2023 Lin, Yang, Wu, Ye, Zhuang, Wang and Tan.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Potential Cul3-involved pathways in NDDs. Schematic illustration of potential Cul3-involved pathways in NDDs. Cul3-KO up-regulates RhoA, leading to dysregulation of the neuronal cytoskeleton and neurogenesis. Cul3 deficiency also up-regulates eIF4G1, promoting cap-dependent translation. Smyd3 also plays as the downstream target of Cul3, which causes NMDAR dysfunction. Additionally, Cul3-KO up-regulates Plastin3, which controls neuronal migration. Furthermore, the COP9 signalosome (CSN) restricts dendritic branching by Cul3-dependent degradation of the actin cross-linked BTB domain protein Kelch. Cul3 deficiency results in Kelch accumulation and uncontrolled dendritic branching. Cul3-KO controls neuronal migration by increasing Plastin3.