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本文引用的文献

1
HBO1 histone acetylase activity is essential for DNA replication licensing and inhibited by Geminin.HBO1 组蛋白乙酰转移酶活性对于 DNA 复制的许可至关重要,并受到 Geminin 的抑制。
Mol Cell. 2010 Jan 15;37(1):57-66. doi: 10.1016/j.molcel.2009.12.012.
2
Cdc7 kinase - a new target for drug development.Cdc7 激酶——药物研发的新靶点。
Eur J Cancer. 2010 Jan;46(1):33-40. doi: 10.1016/j.ejca.2009.09.020.
3
Phosphorylation of Mcm2 by Cdc7 promotes pre-replication complex assembly during cell-cycle re-entry.细胞周期重新进入时,Cdc7对Mcm2的磷酸化作用促进前复制复合体的组装。
Mol Cell. 2009 Jul 31;35(2):206-16. doi: 10.1016/j.molcel.2009.06.014.
4
Docking of a specialized PIP Box onto chromatin-bound PCNA creates a degron for the ubiquitin ligase CRL4Cdt2.将一个特殊的增殖细胞核抗原相互作用基序(PIP Box)对接至与染色质结合的增殖细胞核抗原(PCNA)上,会为泛素连接酶Cullin4-DDB1-Cdt2(CRL4Cdt2)创造一个降解结构域。
Mol Cell. 2009 Jul 10;35(1):93-104. doi: 10.1016/j.molcel.2009.05.012.
5
Selective killing of cancer cells by suppression of geminin activity.通过抑制geminin活性选择性杀死癌细胞。
Cancer Res. 2009 Jun 1;69(11):4870-7. doi: 10.1158/0008-5472.CAN-08-4559.
6
Plant geminivirus rep protein induces rereplication in fission yeast.植物双生病毒复制蛋白在裂殖酵母中诱导再复制。
J Virol. 2009 Jul;83(13):6769-78. doi: 10.1128/JVI.02491-08. Epub 2009 Apr 15.
7
Acetylation by GCN5 regulates CDC6 phosphorylation in the S phase of the cell cycle.GCN5介导的乙酰化作用在细胞周期的S期调节CDC6的磷酸化。
Nat Struct Mol Biol. 2009 Apr;16(4):412-20. doi: 10.1038/nsmb.1583. Epub 2009 Apr 3.
8
Redundant and differential regulation of multiple licensing factors ensures prevention of re-replication in normal human cells.多种许可因子的冗余和差异调节确保了正常人类细胞中再复制的预防。
J Cell Sci. 2009 Apr 15;122(Pt 8):1184-91. doi: 10.1242/jcs.041889.
9
Acetylation/deacetylation modulates the stability of DNA replication licensing factor Cdt1.乙酰化/去乙酰化调节DNA复制许可因子Cdt1的稳定性。
J Biol Chem. 2009 Apr 24;284(17):11446-53. doi: 10.1074/jbc.M809394200. Epub 2009 Mar 10.
10
The p21 and PCNA partnership: a new twist for an old plot.p21与增殖细胞核抗原的合作关系:旧情节中的新转折。
Cell Cycle. 2008 Dec 15;7(24):3840-6. doi: 10.4161/cc.7.24.7243. Epub 2008 Dec 21.

DNA 复制许可控制和复制预防。

DNA replication licensing control and rereplication prevention.

机构信息

Department of Biochemistry and Molecular Biology, The University of Texas Medical School at Houston, Houston, TX 77030, USA.

出版信息

Protein Cell. 2010 Mar;1(3):227-36. doi: 10.1007/s13238-010-0032-z. Epub 2010 Feb 23.

DOI:10.1007/s13238-010-0032-z
PMID:21203969
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4875085/
Abstract

Eukaryotic DNA replication is tightly restricted to only once per cell cycle in order to maintain genome stability. Cells use multiple mechanisms to control the assembly of the prereplication complex (pre-RC), a process known as replication licensing. This review focuses on the regulation of replication licensing by posttranslational modifications of the licensing factors, including phosphorylation, ubiquitylation and acetylation. These modifications are critical in establishing the pre-RC complexes as well as preventing rereplication in each cell cycle. The relationship between rereplication and diseases, including cancer and virus infection, is discussed as well.

摘要

真核生物的 DNA 复制在细胞周期中严格限制仅进行一次,以维持基因组稳定性。细胞利用多种机制来控制前复制复合物(pre-RC)的组装,这个过程被称为复制许可。本综述重点介绍了通过许可因子的翻译后修饰(包括磷酸化、泛素化和乙酰化)对复制许可的调控。这些修饰对于建立 pre-RC 复合物以及防止每个细胞周期中的重复复制至关重要。还讨论了重复复制与疾病(包括癌症和病毒感染)之间的关系。