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MINI REVIEW article
Front. Cell Dev. Biol.
Sec. Signaling
Volume 13 - 2025 | doi: 10.3389/fcell.2025.1560940
This article is part of the Research Topic Neuronal Guidance Signaling in Health and Neurological Diseases View all 3 articles
Implications of draxin in neurological disorders
Provisionally accepted- Hamamatsu University School of Medicine, Hamamatsu, Japan
Axon guidance proteins not only play a role in the formation of proper neural circuits but also have other important functions, such as cell survival, migration, and proliferation in the brain. Therefore, mutations in the genes encoding these proteins frequently cause various types of neurological disorders, including psychiatric disorders and neurodegenerative diseases. We previously identified an axon guidance protein, draxin, that is essential for the development of several neural circuits and cell survival in the brain. Recently, the deletion of the draxin gene was identified in an inbred BTBR T + Itpr3 tf /J (BTBR/J) mouse, which is a widely used model of Autism Spectrum Disorder (ASD), suggesting that draxin deletion is a genetic factor for ASD-like characteristics in BTBR/J mice. In this review, I summarize the neuroanatomical abnormalities in draxin knockout mice by comparing them to BTBR/J mice and discuss the possible contributions of draxin to anatomical and behavioral phenotypes in BTBR/J mice.
Keywords: axon guidance, Draxin, BTBR mouse, ASD, Corpus Callosum
Received: 15 Jan 2025; Accepted: 11 Feb 2025.
Copyright: © 2025 Shinmyo. 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:
Yohei Shinmyo, Hamamatsu University School of Medicine, Hamamatsu, Japan
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