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

被引：5
作者：
Ruiz-Reig, Nuria [1 ]
Hakanen, Janne [1 ]
Tissir, Fadel [1 ,2 ]
机构：
[1] Catholic Univ Louvain, Inst Neurosci, Brussels, Belgium
[2] Hamad Bin Khalifa Univ HBKU, Coll Hlth & Life Sci, Doha, Qatar
来源：
NEURAL REGENERATION RESEARCH | 2024年 / 19卷 / 02期
关键词：
brain disorders; cortical malformations; kinesin; microtubules; neurodegeneration; neurodevelopment; MUTATION; MECHANISMS; DISTINCT; DEFECTS; SPINDLE; CELLS; MALFORMATIONS; MICROTUBULES; DOUBLECORTIN; SUPPRESSION;
D O I：
10.4103/1673-5374.375298
中图分类号：
Q2 [细胞生物学];
学科分类号：
071009 ; 090102 ;
摘要：
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.
引用
收藏
页码：375 / 379
页数：5
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