• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

相似文献

1
Subunit Interactions and cooperativity in the microtubule-severing AAA ATPase spastin.微管切割 AAA ATP 酶 spastin 中的亚基相互作用和协同性。
J Biol Chem. 2012 Jul 27;287(31):26278-90. doi: 10.1074/jbc.M111.291898. Epub 2012 May 27.
2
The nucleotide cycle of spastin correlates with its microtubule-binding properties.动力蛋白激活蛋白的核苷酸循环与其微管结合特性相关。
FEBS J. 2013 Aug;280(16):3868-77. doi: 10.1111/febs.12385. Epub 2013 Jul 12.
3
Structural basis of microtubule severing by the hereditary spastic paraplegia protein spastin.遗传性痉挛性截瘫蛋白spastin切断微管的结构基础。
Nature. 2008 Jan 17;451(7176):363-7. doi: 10.1038/nature06482.
4
Linking axonal degeneration to microtubule remodeling by Spastin-mediated microtubule severing.通过Spastin介导的微管切断将轴突退变与微管重塑联系起来。
J Cell Biol. 2005 Feb 14;168(4):599-606. doi: 10.1083/jcb.200409058.
5
The AAA protein spastin possesses two levels of basal ATPase activity.AAA 蛋白 spastin 具有两个基础 ATP 酶活性水平。
FEBS Lett. 2018 May;592(10):1625-1633. doi: 10.1002/1873-3468.13075. Epub 2018 May 15.
6
Hereditary spastic paraplegia SPG4: what is known and not known about the disease.遗传性痉挛性截瘫SPG4:关于该疾病已知和未知的情况
Brain. 2015 Sep;138(Pt 9):2471-84. doi: 10.1093/brain/awv178. Epub 2015 Jun 20.
7
Evaluation of loss of function as an explanation for SPG4-based hereditary spastic paraplegia.评估功能丧失作为 SPG4 型遗传性痉挛性截瘫的解释。
Hum Mol Genet. 2010 Jul 15;19(14):2767-79. doi: 10.1093/hmg/ddq177. Epub 2010 Apr 29.
8
Recognition of C-terminal amino acids in tubulin by pore loops in Spastin is important for microtubule severing.Spastin中的孔环对微管蛋白C末端氨基酸的识别对于微管切断很重要。
J Cell Biol. 2007 Mar 26;176(7):995-1005. doi: 10.1083/jcb.200610072.
9
The C. elegans homologue of the spastic paraplegia protein, spastin, disassembles microtubules.痉挛性截瘫蛋白spastin的秀丽隐杆线虫同源物可拆解微管。
Biochem Biophys Res Commun. 2007 Jul 20;359(1):157-62. doi: 10.1016/j.bbrc.2007.05.086. Epub 2007 May 22.
10
The AAA ATPase spastin links microtubule severing to membrane modelling.AAA型ATP酶痉挛蛋白将微管切断与膜重塑联系起来。
Biochim Biophys Acta. 2012 Jan;1823(1):192-7. doi: 10.1016/j.bbamcr.2011.08.010. Epub 2011 Aug 25.

引用本文的文献

1
Comprehensive analysis of the human ESCRT-III-MIT domain interactome reveals new cofactors for cytokinetic abscission.全面分析人类 ESCRT-III-MIT 结构域相互作用组揭示了细胞有丝分裂后期分离的新辅助因子。
Elife. 2022 Sep 15;11:e77779. doi: 10.7554/eLife.77779.
2
FBXL17/spastin axis as a novel therapeutic target of hereditary spastic paraplegia.FBXL17/痉挛素轴作为遗传性痉挛性截瘫的新型治疗靶点。
Cell Biosci. 2022 Jul 22;12(1):110. doi: 10.1186/s13578-022-00851-1.
3
The Role of Spastin in Axon Biology.痉挛素在轴突生物学中的作用。
Front Cell Dev Biol. 2022 Jul 5;10:934522. doi: 10.3389/fcell.2022.934522. eCollection 2022.
4
In Vitro Reconstitution of Microtubule Dynamics and Severing Imaged by Label-Free Interference-Reflection Microscopy.无标记干涉反射显微镜对微管动力学和切割的体外重建成像。
Methods Mol Biol. 2022;2430:73-91. doi: 10.1007/978-1-0716-1983-4_5.
5
Cutting, Amplifying, and Aligning Microtubules with Severing Enzymes.用切断酶切割、扩增和对齐微管。
Trends Cell Biol. 2021 Jan;31(1):50-61. doi: 10.1016/j.tcb.2020.10.004. Epub 2020 Nov 9.
6
The molecular principles governing the activity and functional diversity of AAA+ proteins.调控 AAA+ 蛋白活性和功能多样性的分子原理。
Nat Rev Mol Cell Biol. 2020 Jan;21(1):43-58. doi: 10.1038/s41580-019-0183-6. Epub 2019 Nov 21.
7
An allosteric network in spastin couples multiple activities required for microtubule severing.朊病毒蛋白通过别构网络将微管切割所需的多种活性偶联在一起。
Nat Struct Mol Biol. 2019 Aug;26(8):671-678. doi: 10.1038/s41594-019-0257-3. Epub 2019 Jul 8.
8
Hereditary spastic paraplegia: gain-of-function mechanisms revealed by new transgenic mouse.遗传性痉挛性截瘫:新型转基因小鼠揭示的功能获得机制。
Hum Mol Genet. 2019 Apr 1;28(7):1136-1152. doi: 10.1093/hmg/ddy419.
9
Microtubule-severing enzymes: From cellular functions to molecular mechanism.微管切割酶:从细胞功能到分子机制。
J Cell Biol. 2018 Dec 3;217(12):4057-4069. doi: 10.1083/jcb.201612104. Epub 2018 Oct 29.
10
Functional differences of short and long isoforms of spastin harboring missense mutation.具有错义突变的 spastin 短和长异构体的功能差异。
Dis Model Mech. 2018 Sep 10;11(9):dmm033704. doi: 10.1242/dmm.033704.

本文引用的文献

1
A primer to scaffolded DNA origami.支架 DNA 折纸术入门。
Nat Methods. 2011 Mar;8(3):221-9. doi: 10.1038/nmeth.1570.
2
Coupling ATP utilization to protein remodeling by ClpB, a hexameric AAA+ protein.通过 ClpB(六聚体 AAA+ 蛋白)将 ATP 利用与蛋白质重塑相偶联。
Proc Natl Acad Sci U S A. 2009 Dec 29;106(52):22233-8. doi: 10.1073/pnas.0911937106. Epub 2009 Nov 25.
3
Automated comparative protein structure modeling with SWISS-MODEL and Swiss-PdbViewer: a historical perspective.使用SWISS-MODEL和Swiss-PdbViewer进行自动比较蛋白质结构建模:历史视角。
Electrophoresis. 2009 Jun;30 Suppl 1:S162-73. doi: 10.1002/elps.200900140.
4
Properties of the kinesin-3 NcKin3 motor domain and implications for neck function.驱动蛋白-3 NcKin3运动结构域的特性及其对颈部功能的影响。
FEBS J. 2009 Jul;276(13):3641-55. doi: 10.1111/j.1742-4658.2009.07083.x. Epub 2009 May 28.
5
Membrane scission by the ESCRT-III complex.ESCRT-III复合物介导的膜分裂
Nature. 2009 Mar 12;458(7235):172-7. doi: 10.1038/nature07836. Epub 2009 Feb 22.
6
Molecular biology: Concealed enzyme coordination.分子生物学:隐蔽的酶协同作用。
Nature. 2009 Jan 22;457(7228):392-3. doi: 10.1038/457392a.
7
Structural basis for midbody targeting of spastin by the ESCRT-III protein CHMP1B.ESCRT-III蛋白CHMP1B介导痉挛素定位于中体的结构基础。
Nat Struct Mol Biol. 2008 Dec;15(12):1278-86. doi: 10.1038/nsmb.1512. Epub 2008 Nov 9.
8
The 'glutamate switch' provides a link between ATPase activity and ligand binding in AAA+ proteins.“谷氨酸开关”在AAA+蛋白中提供了ATP酶活性与配体结合之间的联系。
Nat Struct Mol Biol. 2008 Nov;15(11):1223-7. doi: 10.1038/nsmb.1501. Epub 2008 Oct 12.
9
Unique rotary ATP synthase and its biological diversity.独特的旋转式ATP合酶及其生物多样性。
Annu Rev Biophys. 2008;37:43-64. doi: 10.1146/annurev.biophys.37.032807.130018.
10
Coupling and dynamics of subunits in the hexameric AAA+ chaperone ClpB.六聚体AAA+伴侣蛋白ClpB中亚基的偶联与动力学
J Mol Biol. 2008 Apr 18;378(1):178-90. doi: 10.1016/j.jmb.2008.02.026. Epub 2008 Feb 21.

微管切割 AAA ATP 酶 spastin 中的亚基相互作用和协同性。

Subunit Interactions and cooperativity in the microtubule-severing AAA ATPase spastin.

机构信息

Department of Physics E22 (Biophysics), Technische Universität München, James-Franck-Strasse 1, D-85748 Garching/Munich, Germany.

出版信息

J Biol Chem. 2012 Jul 27;287(31):26278-90. doi: 10.1074/jbc.M111.291898. Epub 2012 May 27.

DOI:10.1074/jbc.M111.291898
PMID:22637577
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3406712/
Abstract

Spastin is a hexameric ring AAA ATPase that severs microtubules. To see whether the ring complex funnels the energy of multiple ATP hydrolysis events to the site of mechanical action, we investigate here the cooperativity of spastin. Several lines of evidence indicate that interactions among two subunits dominate the cooperative behavior: (i) the ATPase activity shows a sigmoidal dependence on the ATP concentration; (ii) ATPγS displays a mixed-inhibition behavior for normal ATP turnover; and (iii) inactive mutant subunits inhibit the activity of spastin in a hyperbolic dependence, characteristic for two interacting species. A quantitative model based on neighbor interactions fits mutant titration experiments well, suggesting that each subunit is mainly influenced by one of its neighbors. These observations are relevant for patients suffering from SPG4-type hereditary spastic paraplegia and explain why single amino acid exchanges lead to a dominant negative phenotype. In severing assays, wild type spastin is even more sensitive toward the presence of inactive mutants than in enzymatic assays, suggesting a weak coupling of ATPase and severing activity.

摘要

Spastin 是一种六聚体环 AAA ATP 酶,可切断微管。为了观察环复合物是否将多个 ATP 水解事件的能量传递到机械作用部位,我们在此研究 spastin 的协同作用。有几条证据表明,两个亚基之间的相互作用主导着协同行为:(i)ATP 酶活性对 ATP 浓度呈 S 形依赖性;(ii)ATPγS 对正常 ATP 周转显示出混合抑制行为;(iii)无活性突变体亚基以双曲线依赖性抑制 spastin 的活性,这是两种相互作用物质的特征。基于邻接相互作用的定量模型很好地拟合了突变体滴定实验,表明每个亚基主要受其一个邻接的影响。这些观察结果与患有 SPG4 型遗传性痉挛性截瘫的患者有关,并解释了为什么单个氨基酸交换会导致显性负表型。在切断实验中,野生型 spastin 比在酶实验中对无活性突变体的存在更为敏感,这表明 ATP 酶和切断活性之间的耦合较弱。