Glycogen Synthase Kinase 3 Beta (GSK3β) at the Tip of Neuronal Development and Regeneration

被引:85
|
作者
Seira, Oscar [1 ,2 ,3 ]
Antonio del Rio, Jose [1 ,2 ,3 ]
机构
[1] Univ Barcelona, Inst Bioengn Catalonia IBEC, E-08028 Barcelona, Spain
[2] Univ Barcelona, Fac Biol, Dept Cell Biol, E-08028 Barcelona, Spain
[3] Ctr Invest Biomed Red Enfermedades Neurodegenerat, Barcelona 08028, Spain
关键词
Neuritogenesis; Axonal injury; Neurite outgrowth inhibition; Microtubule-associated protein; Actin cytoskeleton; CHONDROITIN-SULFATE PROTEOGLYCAN; SPINAL-CORD-INJURY; NOGO RECEPTOR; AXON GROWTH; NEURITE OUTGROWTH; SEMAPHORIN; 3A; GENE-EXPRESSION; SENSORY NEURONS; EXTRACELLULAR-MATRIX; FUNCTIONAL RECEPTOR;
D O I
10.1007/s12035-013-8571-y
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
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.
引用
收藏
页码:931 / 944
页数:14
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