PERK, mTORC1 and eEF2 interplay during long term potentiation: An Editorial for 'Genetic removal of eIF2a kinase PERK in mice enables hippocampal L-LTP independent of mTORC1 activity' on page 133.

被引：3

作者：

Bevilaqua, Lia R. M. ^{[1
]}

Cammarota, Martin ^{[1
]}

机构：

[1] Univ Fed Rio Grande do Norte, Inst Brain, Memory Res Lab, Ave Nascimento de Castro 2155, BR-59056450 Natal, RN, Brazil

来源：

JOURNAL OF NEUROCHEMISTRY | 2018年 / 146卷 / 02期

关键词：

SYNAPTIC PLASTICITY; PHOSPHORYLATION; TRANSLATION;

D O I：

10.1111/jnc.14485

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

This Editorial highlights a study by Zimmermann and coworkers in the current issue of Journal of Neurochemistry. The authors' link suppression of PKR-like endoplasmatic reticulum kinase (PERK) activity to eukaryotic elongation factor 2 (eEF2) dephosphorylation and mTORC1-independent high-frequency stimulation (HFS)-induced long-term potentiation (LTP) in acute hippocampal slices from PERK forebrain conditional knockout mice. The results suggest that functional interaction between the signaling pathways controlling different phases of the mRNA translation process is necessary for long-term plasticity in the hippocampus.

引用

页码：119 / 121

页数：3