Proteasome limits plasticity-related signaling to the nucleus in the hippocampus.
Proteasome limits plasticity-related signaling to the nucleus in the hippocampus.
复制标题
蛋白酶体限制了海马细胞核的可塑性相关信号传导。
DOI：
10.1016/j.neulet.2018.09.017
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发表时间：
2018
影响因子：
2.5
通讯作者：
Hegde,AshokN
中科院分区：
文献类型：
--
作者：
Vashisht,Anirudh;Bach,SvitlanaV;Fetterhoff,Dustin;Morgan,JamesW;McGee,Maria;Hegde,AshokN
通过泛素-蛋白酶体途径的蛋白质水解对长期突触可塑性的诱导和维持具有多效性作用。在这项研究中，我们研究了蛋白酶体抑制对晚期长时程增强过程中向细胞核发出信号的影响。当使用阈下L-LTP诱导方案时，蛋白酶体抑制导致细胞核中磷酸化CREB（pCREB）的显著增加。cAMP依赖性蛋白激酶/蛋白激酶A、细胞外信号调节激酶和cGMP依赖性蛋白激酶/蛋白激酶G的抑制剂均阻断了阈下刺激后蛋白酶体抑制介导的核pCREB增加。这些结果奠定了基础，了解一个新的作用，蛋白酶体在限制信号的细胞核中缺乏足够的突触刺激。
Proteolysis by the ubiquitin-proteasome pathway has pleiotropic effects on both induction and maintenance of long-term synaptic plasticity. In this study, we examined the effect of proteasome inhibition on signaling to the nucleus during late-phase long-term potentiation. When a subthreshold L-LTP induction protocol was used, proteasome inhibition led to a significant increase in phosphorylated CREB (pCREB) in the nucleus. Inhibitors of cAMP-dependent protein kinase/protein kinase A, extracellular signal-regulated kinase and cGMP-dependent protein kinase/protein kinase G all blocked the proteasome-inhibition-mediated increase in nuclear pCREB after subthreshold stimulation. These results lay the groundwork for understanding a novel role for the proteasome in limiting signaling to the nucleus in the absence of adequate synaptic stimulation.