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本文引用的文献

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Cell Res. 2008 Jan;18(1):48-63. doi: 10.1038/cr.2008.7.
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BMC Mol Biol. 2007 Apr 25;8:29. doi: 10.1186/1471-2199-8-29.
3
Ataxia telangiectasia mutated (ATM) signaling network is modulated by a novel poly(ADP-ribose)-dependent pathway in the early response to DNA-damaging agents.共济失调毛细血管扩张症突变（ATM）信号网络在对DNA损伤剂的早期反应中由一条新的聚（ADP - 核糖）依赖性途径调节。
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4
ATR signaling mediates an S-phase checkpoint after inhibition of poly(ADP-ribose) polymerase activity.在抑制聚（ADP-核糖）聚合酶活性后，ATR信号传导介导S期检查点。
DNA Repair (Amst). 2007 Jun 1;6(6):742-50. doi: 10.1016/j.dnarep.2006.12.015. Epub 2007 Feb 9.
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Mammalian single-strand break repair: mechanisms and links with chromatin.哺乳动物单链断裂修复：机制及其与染色质的联系
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Discovery of bioactive small-molecule inhibitor of poly adp-ribose polymerase: implications for energy-deficient cells.
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Poly(ADP-ribose). The most elaborate metabolite of NAD+.聚（ADP - 核糖）。NAD⁺最复杂的代谢产物。
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Poly(ADP-ribosyl)ation by PARP-1: 'PAR-laying' NAD+ into a nuclear signal.PARP-1介导的聚（ADP-核糖）基化：将NAD⁺“铺就”为一种核信号。
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Involvement of poly(ADP-ribose) polymerase activity in regulating Chk1-dependent apoptotic cell death.聚（ADP - 核糖）聚合酶活性在调节Chk1依赖性凋亡细胞死亡中的作用。
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N-methyl-N'-nitro-N-nitrosoguanidine activates cell-cycle arrest through distinct mechanisms activated in a dose-dependent manner.N-甲基-N'-硝基-N-亚硝基胍通过以剂量依赖性方式激活的不同机制激活细胞周期停滞。
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聚（ADP-核糖）聚合酶-1（PARP-1）与小鼠成纤维细胞中共济失调毛细血管扩张症突变基因（ATR）之间的相互作用被PARP抑制所阻断。

Interaction between PARP-1 and ATR in mouse fibroblasts is blocked by PARP inhibition.

作者信息

Kedar Padmini S, Stefanick Donna F, Horton Julie K, Wilson Samuel H

机构信息

Laboratory of Structural Biology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA.

出版信息

DNA Repair (Amst). 2008 Nov 1;7(11):1787-98. doi: 10.1016/j.dnarep.2008.07.006. Epub 2008 Aug 22.

DOI:10.1016/j.dnarep.2008.07.006
PMID:18691676
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2585487/
Abstract

Inhibition of PARP activity results in extreme sensitization to MMS-induced cell killing in cultured mouse fibroblasts. In these MMS-treated cells, PARP inhibition is accompanied by an accumulation of S-phase cells that requires signaling by the checkpoint kinase ATR [J.K. Horton, D.F. Stefanick, J.M. Naron, P.S. Kedar, S.H. Wilson, Poly(ADP-ribose) polymerase activity prevents signaling pathways for cell cycle arrest following DNA methylating agent exposure, J. Biol. Chem. 280 (2005) 15773-15785]. Here, we examined mouse fibroblast extracts for formation of a complex that may reflect association between the damage responsive proteins PARP-1 and ATR. Co-immunoprecipitation of PARP-1 and ATR was observed in extracts prepared from MMS-treated cells, but not under conditions of PARP inhibition. Further, our experiments demonstrated PAR-adduction of ATR in extracts from control and MMS-treated cells. An interaction between purified ATR and PARP-1 was similarly demonstrated, suggesting that the observed co-immunoprecipitation of ATR and PARP-1 from cell extracts may be due to a direct interaction between the two enzymes. In addition, purified recombinant ATR is a substrate for poly(ADP-ribosyl)ation by PARP-1, and poly(ADP-ribose) adduction of PARP-1 and ATR resulted in an increase in PARP-1 and ATR co-immunoprecipitation.

摘要

抑制聚（ADP - 核糖）聚合酶（PARP）的活性会导致培养的小鼠成纤维细胞对甲基磺酸甲酯（MMS）诱导的细胞杀伤极度敏感。在这些经MMS处理的细胞中，PARP抑制伴随着S期细胞的积累，这需要检查点激酶ATR发出信号[J.K.霍顿、D.F.斯特凡尼克、J.M.纳伦、P.S.凯达尔、S.H.威尔逊，聚（ADP - 核糖）聚合酶活性可防止DNA甲基化剂暴露后细胞周期停滞的信号通路，《生物化学杂志》280（2005）15773 - 15785]。在此，我们检测了小鼠成纤维细胞提取物中是否形成了一种复合物，该复合物可能反映损伤反应蛋白PARP - 1与ATR之间的关联。在从MMS处理的细胞制备的提取物中观察到了PARP - 1和ATR的共免疫沉淀，但在PARP抑制条件下未观察到。此外，我们的实验证明了在对照细胞和MMS处理细胞的提取物中ATR的PAR加合。同样证明了纯化的ATR与PARP - 1之间存在相互作用，这表明从细胞提取物中观察到的ATR和PARP - 1的共免疫沉淀可能是由于这两种酶之间的直接相互作用。此外，纯化的重组ATR是PARP - 1进行聚（ADP - 核糖基）化的底物，PARP - 1和ATR的聚（ADP - 核糖）加合导致PARP - 1和ATR共免疫沉淀增加。