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延伸因子2的磷酸化:脊椎动物中调节基因表达的关键机制。

Phosphorylation of elongation factor 2: a key mechanism regulating gene expression in vertebrates.

作者信息

Ryazanov A G, Spirin A S

机构信息

Institute of Protein Research, Academy of Sciences, Moscow Region, USSR.

出版信息

New Biol. 1990 Oct;2(10):843-50.

PMID:1964087
Abstract

Elongation factor 2 (eEF-2) is a 100-kD protein that catalyzes the ribosomal translocation reaction, resulting in the movement of ribosomes along mRNA. eEF-2 is the target for a very specific Ca2+/calmodulin-dependent eEF-2 kinase. Phosphorylation of eEF-2 makes it inactive in translation, which suggests that protein synthesis can be regulated by Ca2+ through eEF-2 phosphorylation. Recent data demonstrate that eEF-2 phosphorylation can be involved in cell-cycle regulation and other processes where changes of intracellular Ca2+ concentration induce a new physiological state of a cell. The main role of eEF-2 phosphorylation in these processes is temporary inhibition of overall translation in response to transient elevation of the Ca2+ concentrations in the cytoplasm. Temporary inhibition of translation may trigger the transition of a cell from one physiologic state into another because of the disappearance of short-lived repressors and thus the activation of expression of new genes.

摘要

延伸因子2(eEF-2)是一种100千道尔顿的蛋白质,它催化核糖体易位反应,导致核糖体沿信使核糖核酸(mRNA)移动。eEF-2是一种非常特殊的钙/钙调蛋白依赖性eEF-2激酶的作用靶点。eEF-2的磷酸化使其在翻译过程中失活,这表明蛋白质合成可通过eEF-2磷酸化受钙离子调节。最近的数据表明,eEF-2磷酸化可能参与细胞周期调控以及其他细胞内钙离子浓度变化诱导细胞进入新生理状态的过程。eEF-2磷酸化在这些过程中的主要作用是响应细胞质中钙离子浓度的短暂升高而暂时抑制整体翻译。由于短命阻遏物的消失以及新基因表达的激活,翻译的暂时抑制可能会触发细胞从一种生理状态转变为另一种生理状态。

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