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hnRNP K 的缺失会损害海马神经元中的突触可塑性。

Loss of hnRNP K impairs synaptic plasticity in hippocampal neurons.

机构信息

CNR Institute of Neuroscience, Department of Medical Biotechnology and Translational Medicine (BIOMETRA), University of Milan, Milan 20129, Italy.

CNR Institute of Neuroscience, Department of Medical Biotechnology and Translational Medicine (BIOMETRA), University of Milan, Milan 20129, Italy, Department of Brain and Behavioral Sciences, Neurophysiology Unit, University of Pavia, Pavia 27100, Italy, Brain Connectivity Center, C. Mondino National Neurological Institute, Pavia 27100, Italy, and.

出版信息

J Neurosci. 2014 Jul 2;34(27):9088-95. doi: 10.1523/JNEUROSCI.0303-14.2014.

Abstract

Heterogeneous nuclear ribonucleoprotein K (hnRNP K) is an RNA-binding protein implicated in RNA metabolism. Here, we investigated the role of hnRNP K in synapse function. We demonstrated that hnRNP K regulates dendritic spine density and long-term potentiation (LTP) in cultured hippocampal neurons from embryonic rats. LTP requires the extracellular signal-regulated kinase (ERK)1/2-mediated phosphorylation and cytoplasmic accumulation of hnRNP K. Moreover, hnRNP K knockdown prevents ERK cascade activation and GluA1-S845 phosphorylation and surface delivery, which are essential steps for LTP. These findings establish hnRNP K as a new critical regulator of synaptic transmission and plasticity in hippocampal neurons.

摘要

异质核核糖核蛋白 K(hnRNP K)是一种与 RNA 代谢相关的 RNA 结合蛋白。在这里,我们研究了 hnRNP K 在突触功能中的作用。我们证明 hnRNP K 调节胚胎大鼠海马神经元培养物中的树突棘密度和长时程增强(LTP)。LTP 需要细胞外信号调节激酶(ERK)1/2 介导的 hnRNP K 的磷酸化和细胞质积累。此外,hnRNP K 敲低可防止 ERK 级联激活以及 GluA1-S845 磷酸化和表面转运,这对于 LTP 是必不可少的步骤。这些发现将 hnRNP K 确立为海马神经元中突触传递和可塑性的新的关键调节因子。

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