Regulation of Rad6/Rad18 Activity During DNA Damage Tolerance.
Regulation of Rad6/Rad18 Activity During DNA Damage Tolerance.
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DOI：
10.1146/annurev-biophys-060414-033841
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发表时间：
2015
影响因子：
12.4
通讯作者：
Benkovic SJ
中科院分区：
文献类型：
--
作者：
Hedglin M;Benkovic SJ
复制型聚合酶（pols）不能适应受损的模板碱基，当在S期遇到这种进攻时，这些pols就会停止。而不是修复受损的碱基，复制过去可能会通过两个DNA损伤耐受（DDT）途径之一进行，允许复制DNA合成恢复。在translesion DNA合成（TLS）中，一个专门的TLS聚合物被招募来催化稳定的，但往往是错误的，核苷酸掺入相对受损的模板碱基。在模板转换中，新合成的姐妹链被用作无损伤模板以合成通过损伤。在真核生物中，这两种途径都是通过不同的E2/E3对泛素与PCNA滑动夹的缀合来调节的。而由Rad6/Rad18介导的单泛素化介导TLS，通过Ubc13-Mms2/Rad5将该泛素延伸为多聚泛素链将DDT路由到模板转换途径。本文就Rad6/Rad18对PCNA的单泛素化作用及其调控机制进行综述。
Replicative polymerases (pols) cannot accommodate damaged template bases, and these pols stall when such offenses are encountered during S phase. Rather than repairing the damaged base, replication past it may proceed via one of two DNA damage tolerance (DDT) pathways, allowing replicative DNA synthesis to resume. In translesion DNA synthesis (TLS), a specialized TLS pol is recruited to catalyze stable, yet often erroneous, nucleotide incorporation opposite damaged template bases. In template switching, the newly synthesized sister strand is used as a damage-free template to synthesize past the lesion. In eukaryotes, both pathways are regulated by the conjugation of ubiquitin to the PCNA sliding clamp by distinct E2/E3 pairs. Whereas monoubiquitination by Rad6/Rad18 mediates TLS, extension of this ubiquitin to a polyubiquitin chain by Ubc13-Mms2/Rad5 routes DDT to the template switching pathway. In this review, we focus on the monoubiquitination of PCNA by Rad6/Rad18 and summarize the current knowledge of how this process is regulated.
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DOI：
10.1073/pnas.1106136108
发表时间：
2011-06-14
影响因子：
11.1
作者：
Emanuele, Michael J.;Ciccia, Alberto;Elledge, Stephen J.
通讯作者：
Elledge, Stephen J.
影响因子：
7.5
作者：
Boos, Dominik;Frigola, Jordi;Diffley, John F. X.
通讯作者：
Diffley, John F. X.
影响因子：
64.8
作者：
通讯作者：
--
影响因子：
16
作者：
Centore, Richard C.;Yazinski, Stephanie A.;Tse, Alice;Zou, Lee
通讯作者：
Zou, Lee
影响因子：
3.3
作者：
Finley, Daniel;Ulrich, Helle D.;Kaiser, Peter
通讯作者：
Kaiser, Peter