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本文引用的文献

1
SDE2 integrates into the TIMELESS-TIPIN complex to protect stalled replication forks.SDE2 整合到 TIMESLESS-TIPIN 复合物中以保护停滞的复制叉。
Nat Commun. 2020 Oct 30;11(1):5495. doi: 10.1038/s41467-020-19162-5.
2
Cryo-EM Structure of the Fork Protection Complex Bound to CMG at a Replication Fork.与复制叉处的CMG结合的叉保护复合物的冷冻电镜结构
Mol Cell. 2020 Jun 4;78(5):926-940.e13. doi: 10.1016/j.molcel.2020.04.012. Epub 2020 May 4.
3
Overexpression of Claspin and Timeless protects cancer cells from replication stress in a checkpoint-independent manner.Claspin 和 Timeless 的过表达以一种检查点独立的方式保护癌细胞免受复制应激。
Nat Commun. 2019 Feb 22;10(1):910. doi: 10.1038/s41467-019-08886-8.
4
Conditional degradation of SDE2 by the Arg/N-End rule pathway regulates stress response at replication forks.通过 Arg/N-End 规则途径条件性降解 SDE2 可调节复制叉处的应激反应。
Nucleic Acids Res. 2019 May 7;47(8):3996-4010. doi: 10.1093/nar/gkz054.
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Replication Fork Reversal: Players and Guardians.复制叉反转：参与者与守护者
Mol Cell. 2017 Dec 7;68(5):830-833. doi: 10.1016/j.molcel.2017.11.022.
6
PCNA-Dependent Cleavage and Degradation of SDE2 Regulates Response to Replication Stress.PCNA 依赖的 SDE2 切割与降解调控对复制应激的反应
PLoS Genet. 2016 Dec 1;12(12):e1006465. doi: 10.1371/journal.pgen.1006465. eCollection 2016 Dec.
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Laying a trap to kill cancer cells: PARP inhibitors and their mechanisms of action.诱杀癌细胞：PARP 抑制剂及其作用机制。
Sci Transl Med. 2016 Oct 26;8(362):362ps17. doi: 10.1126/scitranslmed.aaf9246.
8
Local and global functions of Timeless and Tipin in replication fork protection.Timeless 和 Tipin 在复制叉保护中的局部和全局功能。
Cell Cycle. 2012 Nov 1;11(21):3945-55. doi: 10.4161/cc.21989. Epub 2012 Sep 17.
9
Maintaining genome stability at the replication fork.在复制叉处维持基因组稳定性。
Nat Rev Mol Cell Biol. 2010 Mar;11(3):208-19. doi: 10.1038/nrm2852.
10
The many facets of the Tim-Tipin protein families' roles in chromosome biology.Tim-Tipin 蛋白家族在染色体生物学中的多种作用。
Cell Cycle. 2010 Feb 15;9(4):700-5. doi: 10.4161/cc.9.4.10676. Epub 2010 Feb 17.

SDE2和TIMELESS在活跃和停滞的DNA复制叉处的作用。

Roles of SDE2 and TIMELESS at active and stalled DNA replication forks.

作者信息

Lo Natalie, Rageul Julie, Kim Hyungjin

机构信息

Department of Pharmacological Sciences, The State University of New York at Stony Brook, Stony Brook, NY, USA.

Stony Brook Cancer Center, Renaissance School of Medicine at Stony Brook University, Stony Brook, NY, USA.

出版信息

Mol Cell Oncol. 2020 Dec 14;8(1):1855053. doi: 10.1080/23723556.2020.1855053. eCollection 2021.

DOI:10.1080/23723556.2020.1855053
PMID:33553608
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7849734/
Abstract

The fork protection complex (FPC), comprising the TIMELESS (TIM)-TIPIN heterodimer, acts as a scaffold of the replisome to support seamless DNA replication. We recently showed that SDE2, a PCNA-associated DNA replication stress regulator, maintains the integrity of the FPC, and together with TIM, protects stalled replication forks from nucleolytic degradation.

摘要

叉形保护复合体（FPC）由TIMELESS（TIM）-TIPIN异二聚体组成，作为复制体的支架来支持无缝DNA复制。我们最近发现，SDE2是一种与增殖细胞核抗原（PCNA）相关的DNA复制应激调节剂，它维持FPC的完整性，并与TIM一起保护停滞的复制叉不被核酸酶降解。