中国神经再生研究(英文版) ›› 2024, Vol. 19 ›› Issue (2): 375-379.doi: 10.4103/1673-5374.375298

• 综述:周围神经损伤修复保护与再生 • 上一篇    下一篇

连接神经发育与神经退行性变:聚焦驱动蛋白超家族蛋白 2A (KIF2A) 的作用

  

  • 出版日期:2024-02-15 发布日期:2023-08-30

Connecting neurodevelopment to neurodegeneration: a spotlight on the role of kinesin superfamily protein 2A (KIF2A)

Nuria Ruiz-Reig1, Janne Hakanen1, Fadel Tissir1, 2, *    

  1. 1Université catholique de Louvain, Institute of neuroscience, Brussels, Belgium; 2College of Health and Life Sciences, Hamad Bin Khalifa University (HBKU), Doha, Qatar
  • Online:2024-02-15 Published:2023-08-30
  • Contact: Fadel Tissir, PhD, ftissir@hbku.edu.qa.
  • Supported by:
    This work was supported by the following grants: Fund for Scientific Research (FNRS) PDR T0236.20, FNRS-Exellence of Science 30913351, and FNRS CDR J.0175.23 (to FT).

摘要: https://orcid.org/0000-0002-9292-6622 (Fadel Tissir)

Abstract: Microtubules play a central role in cytoskeletal changes during neuronal development and maintenance. Microtubule dynamics is essential to polarity and shape transitions underlying neural cell division, differentiation, motility, and maturation. Kinesin superfamily protein 2A is a member of human kinesin 13 gene family of proteins that depolymerize and destabilize microtubules. In dividing cells, kinesin superfamily protein 2A is involved in mitotic progression, spindle assembly, and chromosome segregation. In postmitotic neurons, it is required for axon/dendrite specification and extension, neuronal migration, connectivity, and survival. Humans with kinesin superfamily protein 2A mutations suffer from a variety of malformations of cortical development, epilepsy, autism spectrum disorder, and neurodegeneration. In this review, we discuss how kinesin superfamily protein 2A regulates neuronal development and function, and how its deregulation causes neurodevelopmental and neurological disorders.

Key words: brain disorders, cortical malformations, kinesin, microtubules, neurodegeneration, neurodevelopment