神经元发育：SAD 激酶让轴突变得快乐。
Neuronal development: SAD kinases make happy axons.
机构信息
Neuroscience Center, University of North Carolina School of Medicine, Chapel Hill, NC 27599, USA.
出版信息
Curr Biol. 2013 Sep 9;23(17):R720-3. doi: 10.1016/j.cub.2013.07.073.
Abstract
The polarity proteins LKB1 and SAD-A/B are key regulators of axon specification in the developing cerebral cortex. Recent studies now show that this mechanism cannot be generalized to other classes of neurons: instead, SAD-A/B functions downstream of neurotrophin signaling in sensory neurons to mediate a later stage of axon development - arborization in the target field.
摘要
极性蛋白 LKB1 和 SAD-A/B 是大脑皮层发育中轴突特化的关键调节因子。最近的研究表明，这一机制不能推广到其他神经元类别：相反，SAD-A/B 在感觉神经元中的神经营养因子信号下游发挥作用，以介导轴突发育的后期阶段——在靶场的分支。
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