• 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

非洲爪蟾无细胞提取物中M期退出时细胞周期蛋白依赖性激酶1/细胞周期蛋白B失活的经典途径和替代途径

Canonical and Alternative Pathways in Cyclin-Dependent Kinase 1/Cyclin B Inactivation upon M-Phase Exit in Xenopus laevis Cell-Free Extracts.

作者信息

Kubiak Jacek Z, El Dika Mohammed

机构信息

Cell Cycle Group, Institute of Genetics & Development, University of Rennes 1, CNRS-UMR 6061, Faculty of Medicine, 2 Avenue Prof. Léon Bernard, CS 34317, 35043 Rennes Cedex, France.

出版信息

Enzyme Res. 2011;2011:523420. doi: 10.4061/2011/523420. Epub 2011 Jun 22.

DOI:10.4061/2011/523420
PMID:21755042
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3132491/
Abstract

Cyclin-Dependent Kinase 1 (CDK1) is the major M-phase kinase known also as the M-phase Promoting Factor or MPF. Studies performed during the last decade have shown many details of how CDK1 is regulated and also how it regulates the cell cycle progression. Xenopus laevis cell-free extracts were widely used to elucidate the details and to obtain a global view of the role of CDK1 in M-phase control. CDK1 inactivation upon M-phase exit is a primordial process leading to the M-phase/interphase transition during the cell cycle. Here we discuss two closely related aspects of CDK1 regulation in Xenopus laevis cell-free extracts: firstly, how CDK1 becomes inactivated and secondly, how other actors, like kinases and phosphatases network and/or specific inhibitors, cooperate with CDK1 inactivation to assure timely exit from the M-phase.

摘要

细胞周期蛋白依赖性激酶1(CDK1)是主要的M期激酶,也被称为M期促进因子或MPF。过去十年进行的研究揭示了CDK1如何被调控以及它如何调控细胞周期进程的许多细节。非洲爪蟾无细胞提取物被广泛用于阐明这些细节,并全面了解CDK1在M期控制中的作用。M期退出时CDK1的失活是细胞周期中导致M期/间期转换的一个原始过程。在此,我们讨论非洲爪蟾无细胞提取物中CDK1调控的两个密切相关的方面:第一,CDK1如何失活;第二,其他因子,如激酶和磷酸酶网络及/或特定抑制剂,如何与CDK1失活协同作用,以确保及时退出M期。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0586/3132491/a7516f7c7905/ER2011-523420.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0586/3132491/1841a77cd7e2/ER2011-523420.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0586/3132491/46341bd33232/ER2011-523420.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0586/3132491/a7516f7c7905/ER2011-523420.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0586/3132491/1841a77cd7e2/ER2011-523420.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0586/3132491/46341bd33232/ER2011-523420.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0586/3132491/a7516f7c7905/ER2011-523420.003.jpg

相似文献

1
Canonical and Alternative Pathways in Cyclin-Dependent Kinase 1/Cyclin B Inactivation upon M-Phase Exit in Xenopus laevis Cell-Free Extracts.非洲爪蟾无细胞提取物中M期退出时细胞周期蛋白依赖性激酶1/细胞周期蛋白B失活的经典途径和替代途径
Enzyme Res. 2011;2011:523420. doi: 10.4061/2011/523420. Epub 2011 Jun 22.
2
Cyclin B2/cyclin-dependent kinase1 dissociation precedes CDK1 Thr-161 dephosphorylation upon M-phase promoting factor inactivation in Xenopus laevis cell-free extract.在非洲爪蟾无细胞提取物中,M期促进因子失活时,细胞周期蛋白B2/细胞周期蛋白依赖性激酶1解离先于细胞周期蛋白依赖性激酶1苏氨酸-161去磷酸化。
Int J Dev Biol. 2007;51(4):297-305. doi: 10.1387/ijdb.072292fc.
3
Role for non-proteolytic control of M-phase-promoting factor activity at M-phase exit.有丝分裂后期非蛋白水解调控 M 期促进因子活性的作用。
PLoS One. 2007 Feb 28;2(2):e247. doi: 10.1371/journal.pone.0000247.
4
Cyclin B dissociation from CDK1 precedes its degradation upon MPF inactivation in mitotic extracts of Xenopus laevis embryos.在非洲爪蟾胚胎的有丝分裂提取物中,MPF失活时,细胞周期蛋白B与细胞周期蛋白依赖性激酶1解离先于其降解。
Cell Cycle. 2006 Aug;5(15):1687-98. doi: 10.4161/cc.5.15.3123. Epub 2006 Aug 1.
5
Proteomics reveals a switch in CDK1-associated proteins upon M-phase exit during the Xenopus laevis oocyte to embryo transition.蛋白质组学揭示了爪蟾卵母细胞到胚胎过渡期间有丝分裂后期 CDK1 相关蛋白的转变。
Int J Biochem Cell Biol. 2012 Jan;44(1):53-64. doi: 10.1016/j.biocel.2011.09.003. Epub 2011 Sep 21.
6
Control of timing of embryonic M-phase entry and exit is differentially sensitive to CDK1 and PP2A balance.胚胎有丝分裂期进入和退出时间的控制对细胞周期蛋白依赖性激酶1(CDK1)和蛋白磷酸酶2A(PP2A)的平衡具有不同的敏感性。
Int J Dev Biol. 2014;58(10-12):767-74. doi: 10.1387/ijdb.140101jk.
7
Inactivation of p42 mitogen-activated protein kinase is required for exit from M-phase after cyclin destruction.细胞周期蛋白破坏后从M期退出需要p42丝裂原活化蛋白激酶失活。
J Biol Chem. 1999 Nov 5;274(45):32085-90. doi: 10.1074/jbc.274.45.32085.
8
Fine tuning the cell cycle: activation of the Cdk1 inhibitory phosphorylation pathway during mitotic exit.精细调控细胞周期:有丝分裂退出过程中Cdk1抑制性磷酸化途径的激活
Mol Biol Cell. 2009 Mar;20(6):1737-48. doi: 10.1091/mbc.e08-07-0771. Epub 2009 Jan 21.
9
CDC6 controls dynamics of the first embryonic M-phase entry and progression via CDK1 inhibition.细胞周期蛋白依赖性激酶6(CDC6)通过抑制细胞周期蛋白依赖性激酶1(CDK1)来控制胚胎第一次有丝分裂期进入和进程的动态变化。
Dev Biol. 2014 Dec 1;396(1):67-80. doi: 10.1016/j.ydbio.2014.09.023. Epub 2014 Oct 1.
10
Differences in regulation of the first two M-phases in Xenopus laevis embryo cell-free extracts.非洲爪蟾胚胎无细胞提取物中前两个M期调控的差异。
Dev Biol. 2005 Sep 15;285(2):358-75. doi: 10.1016/j.ydbio.2005.06.028.

引用本文的文献

1
Epigenetic-Mediated Regulation of Gene Expression for Biological Control and Cancer: Fidelity of Mechanisms Governing the Cell Cycle.基因表达的表观遗传调控与生物控制和癌症:细胞周期调控机制的保真度。
Results Probl Cell Differ. 2022;70:375-396. doi: 10.1007/978-3-031-06573-6_13.
2
Epigenetic-Mediated Regulation of Gene Expression for Biological Control and Cancer: Cell and Tissue Structure, Function, and Phenotype.表观遗传介导的基因表达调控在生物防治和癌症中的作用:细胞和组织的结构、功能和表型。
Results Probl Cell Differ. 2022;70:339-373. doi: 10.1007/978-3-031-06573-6_12.
3
Cyclins and cyclin-dependent kinases: from biology to tumorigenesis and therapeutic opportunities.

本文引用的文献

1
Established and novel Cdk/cyclin complexes regulating the cell cycle and development.调控细胞周期和发育的已确立及新型细胞周期蛋白依赖性激酶/细胞周期蛋白复合物
Results Probl Cell Differ. 2011;53:365-89. doi: 10.1007/978-3-642-19065-0_16.
2
Driving the cell cycle with a minimal CDK control network.用最小的 CDK 控制网络驱动细胞周期。
Nature. 2010 Dec 23;468(7327):1074-9. doi: 10.1038/nature09543.
3
The substrate of Greatwall kinase, Arpp19, controls mitosis by inhibiting protein phosphatase 2A.长城激酶的底物 Arpp19 通过抑制蛋白磷酸酶 2A 来控制有丝分裂。
细胞周期蛋白与细胞周期蛋白依赖性激酶:从生物学特性到肿瘤发生及治疗机遇
J Cancer Res Clin Oncol. 2023 Apr;149(4):1585-1606. doi: 10.1007/s00432-022-04135-6. Epub 2022 Jul 4.
Science. 2010 Dec 17;330(6011):1673-7. doi: 10.1126/science.1197048.
4
Greatwall phosphorylates an inhibitor of protein phosphatase 2A that is essential for mitosis.长城激酶磷酸化了一种蛋白磷酸酶 2A 的抑制剂,这种抑制剂对于有丝分裂是必需的。
Science. 2010 Dec 17;330(6011):1670-3. doi: 10.1126/science.1195689.
5
Cell division cycle 6, a mitotic substrate of polo-like kinase 1, regulates chromosomal segregation mediated by cyclin-dependent kinase 1 and separase.细胞分裂周期蛋白 6,作为 polo 样激酶 1 的有丝分裂底物,调节细胞周期蛋白依赖性激酶 1 和 separase 介导的染色体分离。
Proc Natl Acad Sci U S A. 2010 Nov 16;107(46):19742-7. doi: 10.1073/pnas.1013557107. Epub 2010 Nov 1.
6
The M phase kinase Greatwall (Gwl) promotes inactivation of PP2A/B55delta, a phosphatase directed against CDK phosphosites.M 期激酶 Greatwall(Gwl)促进了针对 CDK 磷酸化位点的磷酸酶 PP2A/B55delta 的失活。
Mol Biol Cell. 2009 Nov;20(22):4777-89. doi: 10.1091/mbc.e09-07-0643. Epub 2009 Sep 30.
7
Regulated activity of PP2A-B55 delta is crucial for controlling entry into and exit from mitosis in Xenopus egg extracts.PP2A-B55δ 的调控活性对于控制非洲爪蟾卵提取物中细胞有丝分裂的进出至关重要。
EMBO J. 2009 Sep 16;28(18):2777-85. doi: 10.1038/emboj.2009.238. Epub 2009 Aug 20.
8
Greatwall maintains mitosis through regulation of PP2A.长城通过调节蛋白磷酸酶2A维持有丝分裂。
EMBO J. 2009 Sep 16;28(18):2786-93. doi: 10.1038/emboj.2009.228. Epub 2009 Aug 13.
9
Fertilization differently affects the levels of cyclin B1 and M-phase promoting factor activity in maturing and metaphase II mouse oocytes.受精对成熟和中期II期小鼠卵母细胞中细胞周期蛋白B1水平和M期促进因子活性的影响不同。
Reproduction. 2008 Dec;136(6):741-52. doi: 10.1530/REP-08-0271. Epub 2008 Sep 10.
10
Regulation of APC/C activators in mitosis and meiosis.有丝分裂和减数分裂中后期促进复合物/细胞周期体(APC/C)激活因子的调控
Annu Rev Cell Dev Biol. 2008;24:475-99. doi: 10.1146/annurev.cellbio.041408.115949.