Shea Thomas B, Chan Walter K-H
Center for Cellular Neurobiology and Neurodegeneration Research, Department of Biological Sciences, University of Massachusetts Lowell, One University Avenue, Lowell, MA 01854, USA.
Eur J Neurosci. 2008 Apr;27(8):1893-901. doi: 10.1111/j.1460-9568.2008.06165.x.
Neurofilament (NF) phosphorylation has long been considered to regulate axonal transport rate and in doing so to provide stability to mature axons. Studies utilizing mice in which the C-terminal region of NF subunits (which contains the vast majority of phosphorylation sites) has been deleted has prompted an ongoing challenge to this hypothesis. We evaluate the collective evidence to date for and against a role for NF C-terminal phosphorylation in regulation of axonal transport and in providing structural support for axons, including some novel studies from our laboratory. We present a few suggestions for further experimentation in this area, and expand upon previous models for axonal NF dynamics. Finally, we address how C-terminal phosphorylation is regionally and temporally regulated by a balance of kinase and phosphatase activities, and how misregulation of this balance can contribute to motor neuron disease.
长期以来,神经丝(NF)磷酸化一直被认为可调节轴突运输速率,并以此为成熟轴突提供稳定性。利用已删除NF亚基C末端区域(该区域包含绝大多数磷酸化位点)的小鼠开展的研究,对这一假说提出了持续的挑战。我们评估了迄今为止支持和反对NF C末端磷酸化在调节轴突运输及为轴突提供结构支持中发挥作用的综合证据,其中包括我们实验室的一些新研究。我们针对该领域的进一步实验提出了一些建议,并扩展了先前关于轴突NF动态变化的模型。最后,我们阐述了C末端磷酸化如何通过激酶和磷酸酶活性的平衡在区域和时间上受到调节,以及这种平衡的失调如何导致运动神经元疾病。