Kitagishi Yasuko, Minami Akari, Nakanishi Atsuko, Ogura Yasunori, Matsuda Satoru
Department of Food Science and Nutrition, Nara Women's University, Kita-Uoya Nishimachi, Nara 630-8506, Japan.
Int J Mol Sci. 2015 Jan 30;16(2):3095-115. doi: 10.3390/ijms16023095.
A brain-enriched multi-domain scaffolding protein, neurobeachin has been identified as a candidate gene for autism patients. Mutations in the synaptic adhesion protein cell adhesion molecule 1 (CADM1) are also associated with autism spectrum disorder, a neurodevelopmental disorder of uncertain molecular origin. Potential roles of neurobeachin and CADM1 have been suggested to a function of vesicle transport in endosomal trafficking. It seems that protein kinase B (AKT) and cyclic adenosine monophosphate (cAMP)-dependent protein kinase A (PKA) have key roles in the neuron membrane trafficking involved in the pathogenesis of autism. Attention deficit hyperactivity disorder (ADHD) is documented to dopaminergic insufficiencies, which is attributed to synaptic dysfunction of dopamine transporter (DAT). AKT is also essential for the DAT cell-surface redistribution. In the present paper, we summarize and discuss the importance of several protein kinases that regulate the membrane trafficking involved in autism and ADHD, suggesting new targets for therapeutic intervention.
神经海滩蛋白是一种在大脑中高度富集的多结构域支架蛋白，已被确定为自闭症患者的候选基因。突触粘附蛋白细胞粘附分子1（CADM1）的突变也与自闭症谱系障碍有关，这是一种分子起源不明的神经发育障碍。神经海滩蛋白和CADM1的潜在作用被认为与内体运输中的囊泡运输功能有关。蛋白激酶B（AKT）和环磷酸腺苷（cAMP）依赖性蛋白激酶A（PKA）似乎在自闭症发病机制中涉及的神经元膜运输中起关键作用。注意力缺陷多动障碍（ADHD）被证明与多巴胺能不足有关，这归因于多巴胺转运体（DAT）的突触功能障碍。AKT对于DAT细胞表面的重新分布也至关重要。在本文中，我们总结并讨论了几种调节自闭症和ADHD中膜运输的蛋白激酶的重要性，为治疗干预提出了新的靶点。
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