REVIEW article
Front. Cell Dev. Biol.
Sec. Signaling
Volume 13 - 2025 | doi: 10.3389/fcell.2025.1557653
This article is part of the Research TopicNeuronal Guidance Signaling in Health and Neurological DiseasesView all 8 articles
Emerging Roles for E3 Ubiquitin Ligases in Neural Development and Disease
Provisionally accepted
Maya Hale
Greg J. Bashaw*- Department of Neuroscience, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, United States
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Neurodevelopment is an intricate process with highly regulated, overlapping stages including neuronal differentiation and axon guidance. Aberrations during these and other stages are tied to the etiology of neurodevelopmental disorders like Autism Spectrum Disorder, Angelman Syndrome, and X-linked Intellectual Disability. Ubiquitination is a dynamic and highly reversible post-translational modification conferred by E3 ubiquitin ligases. Recent discoveries have advanced the understanding of how substrate ubiquitination can guide protein localization, drive protein degradation, and alter protein post translational modifications. In this review, we highlight members of the RING and HECT E3 ligase families to discuss their novel roles in the molecular mechanisms regulating neurodevelopment. These findings are both instrumental for informing the future directions of neurodevelopmental research, and in expanding knowledge of intracellular mechanisms of protein trafficking. In addition, a deeper understanding of the molecular mechanisms of E3 ligase function in development promises to offer new insights into the pathogenesis of neurodevelopmental disorders.
Keywords: neural differentiation, axon guidance, synapse formation, neural developmental disorders, E3 ubiquitin ligase, commissureless, Ndfip, slit
Received: 08 Jan 2025; Accepted: 25 Apr 2025.
Copyright: © 2025 Hale and Bashaw. 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) or licensor 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.
* Correspondence: Greg J. Bashaw, Department of Neuroscience, Perelman School of Medicine, University of Pennsylvania, Philadelphia, 19104, Pennsylvania, United States
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