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了解糖原合成酶激酶3细胞作用的最新进展。

Recent advances in understanding the cellular roles of GSK-3.

作者信息

Cormier Kevin W, Woodgett James R

机构信息

Lunenfeld-Tanenbaum Research Institute, Sinai Health System, 600 University Avenue, Toronto, ON, M5G 1X5, Canada.

出版信息

F1000Res. 2017 Feb 20;6. doi: 10.12688/f1000research.10557.1. eCollection 2017.

DOI:10.12688/f1000research.10557.1
PMID:28299185
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5321126/
Abstract

Glycogen synthase kinase-3 (GSK-3) is a ubiquitously expressed protein kinase that sits at the nexus of multiple signaling pathways. Its deep integration into cellular control circuits is consummate to its implication in diseases ranging from mood disorders to diabetes to neurodegenerative diseases and cancers. The selectivity and insulation of such a promiscuous kinase from unwanted crosstalk between pathways, while orchestrating a multifaceted response to cellular stimuli, offer key insights into more general mechanisms of cell regulation. Here, we review recent advances that have contributed to the understanding of GSK-3 and its role in driving appreciation of intracellular signal coordination.

摘要

糖原合酶激酶-3(GSK-3)是一种广泛表达的蛋白激酶,处于多种信号通路的核心位置。它深度融入细胞控制回路,这与其在从情绪障碍到糖尿病、神经退行性疾病和癌症等多种疾病中的作用密切相关。在协调细胞对刺激的多方面反应时,这种多用途激酶如何避免与其他通路产生不必要的串扰,实现选择性和隔离性,这为更普遍的细胞调节机制提供了关键见解。在此,我们综述了近期的研究进展,这些进展有助于理解GSK-3及其在促进细胞内信号协调方面的作用。

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A unique type of GSK-3 inhibitor brings new opportunities to the clinic.一种独特类型的糖原合成酶激酶-3(GSK-3)抑制剂为临床带来了新机遇。
Sci Signal. 2016 Nov 15;9(454):ra110. doi: 10.1126/scisignal.aah7102.
2
Effects of mutations in Wnt/β-catenin, hedgehog, Notch and PI3K pathways on GSK-3 activity-Diverse effects on cell growth, metabolism and cancer.Wnt/β-连环蛋白、刺猬信号、Notch和PI3K信号通路中的突变对GSK-3活性的影响——对细胞生长、代谢和癌症的多种影响
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β-Catenin-Independent Roles of Wnt/LRP6 Signaling.β-连环蛋白非依赖性 Wnt/LRP6 信号通路的作用。
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Inactivation of nuclear GSK3β by Ser(389) phosphorylation promotes lymphocyte fitness during DNA double-strand break response.通过Ser(389)磷酸化使核GSK3β失活可促进DNA双链断裂反应期间淋巴细胞的适应性。
Nat Commun. 2016 Jan 29;7:10553. doi: 10.1038/ncomms10553.
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