GSK3 signalling in neural development

被引:707
作者
Hur, Eun-Mi [1 ]
Zhou, Feng-Quan [1 ,2 ]
机构
[1] Johns Hopkins Univ, Sch Med, Dept Orthopaed Surg, Baltimore, MD 21287 USA
[2] Johns Hopkins Univ, Sch Med, Solomon H Snyder Dept Neurosci, Baltimore, MD 21287 USA
基金
美国国家卫生研究院;
关键词
GLYCOGEN-SYNTHASE KINASE-3; ADENOMATOUS POLYPOSIS-COLI; DNA-BINDING ACTIVITY; NEURONAL POLARITY; BETA-CATENIN; SUBSTRATE-SPECIFICITY; MULTISITE PHOSPHORYLATION; AXONAL ELONGATION; RETINOIC ACID; CONE MOTILITY;
D O I
10.1038/nrn2870
中图分类号
Q189 [神经科学];
学科分类号
071006 [神经生物学];
摘要
Recent evidence suggests that glycogen synthase kinase 3 (GSK3) proteins and their upstream and downstream regulators have key roles in many fundamental processes during neurodevelopment. Disruption of GSK3 signalling adversely affects brain development and is associated with several neurodevelopmental disorders. Here, we discuss the mechanisms by which GSK3 activity is regulated in the nervous system and provide an overview of the recent advances in the understanding of how GSK3 signalling controls neurogenesis, neuronal polarization and axon growth during brain development. These recent advances suggest that GSK3 is a crucial node that mediates various cellular processes that are controlled by multiple signalling molecules - for example, disrupted in schizophrenia 1 (DISC1), partitioning defective homologue 3 (PAR3), PAR6 and Wnt proteins - that regulate neurodevelopment.
引用
收藏
页码:539 / 551
页数:13
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