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本文引用的文献

1
Tribbles in the 21st Century: The Evolving Roles of Tribbles Pseudokinases in Biology and Disease.21世纪的 Tribbles:Tribbles 假激酶在生物学和疾病中的角色演变
Trends Cell Biol. 2017 Apr;27(4):284-298. doi: 10.1016/j.tcb.2016.11.002. Epub 2016 Nov 28.
2
The evolving world of pseudoenzymes: proteins, prejudice and zombies.伪酶的演变世界:蛋白质、偏见与僵尸
BMC Biol. 2016 Nov 11;14(1):98. doi: 10.1186/s12915-016-0322-x.
3
Overcoming resistance to HER2 inhibitors through state-specific kinase binding.通过特定状态的激酶结合克服对HER2抑制剂的耐药性。
Nat Chem Biol. 2016 Nov;12(11):923-930. doi: 10.1038/nchembio.2171. Epub 2016 Sep 5.
4
Cerebellar Ataxia and Coenzyme Q Deficiency through Loss of Unorthodox Kinase Activity.非传统激酶活性丧失导致的小脑共济失调和辅酶Q缺乏症。
Mol Cell. 2016 Aug 18;63(4):608-620. doi: 10.1016/j.molcel.2016.06.030. Epub 2016 Aug 4.
5
Mitochondria in lung disease.肺部疾病中的线粒体
J Clin Invest. 2016 Mar 1;126(3):809-20. doi: 10.1172/JCI81113.
6
Molecular Mechanism of CCAAT-Enhancer Binding Protein Recruitment by the TRIB1 Pseudokinase.TRIB1 假激酶募集 CCAAT-增强子结合蛋白的分子机制。
Structure. 2015 Nov 3;23(11):2111-21. doi: 10.1016/j.str.2015.08.017. Epub 2015 Oct 9.
7
Mitochondria: hubs of cellular signaling, energetics and redox balance. A rich, vibrant, and diverse landscape of mitochondrial research.线粒体:细胞信号传导、能量代谢及氧化还原平衡的枢纽。线粒体研究领域丰富、活跃且多样。
Front Physiol. 2015 Mar 26;6:94. doi: 10.3389/fphys.2015.00094. eCollection 2015.
8
Signalling scaffolds and local organization of cellular behaviour.信号支架与细胞行为的局部组织
Nat Rev Mol Cell Biol. 2015 Apr;16(4):232-44. doi: 10.1038/nrm3966. Epub 2015 Mar 18.
9
Mitochondrial ADCK3 employs an atypical protein kinase-like fold to enable coenzyme Q biosynthesis.线粒体ADCK3利用一种非典型的蛋白激酶样结构域来实现辅酶Q的生物合成。
Mol Cell. 2015 Jan 8;57(1):83-94. doi: 10.1016/j.molcel.2014.11.002. Epub 2014 Dec 11.
10
Day of the dead: pseudokinases and pseudophosphatases in physiology and disease.死亡之日:生理学和疾病中的假激酶和假磷酸酶。
Trends Cell Biol. 2014 Sep;24(9):489-505. doi: 10.1016/j.tcb.2014.03.008. Epub 2014 May 10.

伪支架和锚定蛋白:差异在于细节。

Pseudoscaffolds and anchoring proteins: the difference is in the details.

作者信息

Aggarwal-Howarth Stacey, Scott John D

机构信息

Howard Hughes Medical Institute and Department of Pharmacology, University of Washington, Seattle, WA, U.S.A.

出版信息

Biochem Soc Trans. 2017 Apr 15;45(2):371-379. doi: 10.1042/BST20160329.

DOI:10.1042/BST20160329
PMID:28408477
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5497583/
Abstract

Pseudokinases and pseudophosphatases possess the ability to bind substrates without catalyzing their modification, thereby providing a mechanism to recruit potential phosphotargets away from active enzymes. Since many of these pseudoenzymes possess other characteristics such as localization signals, separate catalytic sites, and protein-protein interaction domains, they have the capacity to influence signaling dynamics in local environments. In a similar manner, the targeting of signaling enzymes to subcellular locations by A-kinase-anchoring proteins (AKAPs) allows for precise and local control of second messenger signaling events. Here, we will discuss how pseudoenzymes form 'pseudoscaffolds' and compare and contrast this compartment-specific regulatory role with the signal organization properties of AKAPs. The mitochondria will be the focus of this review, as they are dynamic organelles that influence a broad range of cellular processes such as metabolism, ATP synthesis, and apoptosis.

摘要

假激酶和假磷酸酶具有在不催化底物修饰的情况下结合底物的能力,从而提供一种将潜在磷酸化靶点从活性酶中招募出来的机制。由于许多这类假酶具有其他特征,如定位信号、独立的催化位点和蛋白质-蛋白质相互作用结构域,它们有能力影响局部环境中的信号转导动态。同样,A激酶锚定蛋白(AKAPs)将信号酶靶向亚细胞位置,使得第二信使信号事件能够得到精确的局部控制。在此,我们将讨论假酶如何形成“假支架”,并将这种特定区室的调节作用与AKAPs的信号组织特性进行比较和对比。线粒体将成为本综述的重点,因为它们是动态细胞器,影响着广泛的细胞过程,如代谢、ATP合成和细胞凋亡。