期刊
MOLECULAR NEUROBIOLOGY
卷 49, 期 2, 页码 931-944出版社
SPRINGER
DOI: 10.1007/s12035-013-8571-y
关键词
Neuritogenesis; Axonal injury; Neurite outgrowth inhibition; Microtubule-associated protein; Actin cytoskeleton
资金
- European Commission [222887]
- Spanish Ministry of Science and Innovation [BFU2012-32617]
- Generalitat de Catalunya [SGR2009-366]
- La Caixa Obra Social Foundation (LCOSF)
- Instituto Salud Carlos III [PI11/03028]
- MICINN
- IBEC
- ISCIII (Ciberned)
Gaining a basic understanding of the inhibitory molecules and the intracellular signaling involved in axon development and repulsion after neural lesions is of clear biomedical interest. In recent years, numerous studies have described new molecules and intracellular mechanisms that impair axonal outgrowth after injury. In this scenario, the role of glycogen synthase kinase 3 beta (GSK3 beta) in the axonal responses that occur after central nervous system (CNS) lesions began to be elucidated. GSK3 beta function in the nervous tissue is associated with neural development, neuron polarization, and, more recently, neurodegeneration. In fact, GSK3 beta has been considered as a putative therapeutic target for promoting functional recovery in injured or degenerative CNS. In this review, we summarize current understanding of the role of GSK3 beta during neuronal development and regeneration. In particular, we discuss GSK3 beta activity levels and their possible impact on cytoskeleton dynamics during both processes.
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