Neuron membrane trafficking and protein kinases involved in autism and ADHD.
Neuron membrane trafficking and protein kinases involved in autism and ADHD.
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DOI：
10.3390/ijms16023095
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发表时间：
2015-01-30
影响因子：
5.6
通讯作者：
Matsuda S
中科院分区：
文献类型：
--
作者：
Kitagishi Y;Minami A;Nakanishi A;Ogura Y;Matsuda S
神经海滩蛋白是一种富含大脑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，自闭症谱系障碍是一种分子起源不确定的神经发育障碍。神经海滩蛋白和CADM1的潜在作用已被认为是囊泡运输的功能。蛋白激酶B（AKT）和环磷酸腺苷（cAMP）依赖的蛋白激酶A（PKA）在自闭症发病机制中的神经元膜运输中起关键作用。注意缺陷多动障碍（ADHD）是一种多巴胺能神经元障碍，其主要原因是多巴胺转运蛋白（DAT）的突触功能障碍。AKT对DAT细胞表面的再分布也至关重要。在本文中，我们总结和讨论了几种蛋白激酶的重要性，调节膜贩运参与自闭症和多动症，提出了新的治疗干预的目标。
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.
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