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PARP 家族酶:多聚(ADP-核糖)翻译后修饰的调节和催化。

PARP family enzymes: regulation and catalysis of the poly(ADP-ribose) posttranslational modification.

机构信息

Department of Biochemistry and Molecular Medicine, Université de Montréal, Montréal, Québec, Canada.

Department of Biochemistry and Molecular Medicine, Université de Montréal, Montréal, Québec, Canada.

出版信息

Curr Opin Struct Biol. 2018 Dec;53:187-198. doi: 10.1016/j.sbi.2018.11.002. Epub 2018 Nov 24.

DOI:10.1016/j.sbi.2018.11.002
PMID:30481609
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6687463/
Abstract

Poly(ADP-ribose) is a posttranslational modification and signaling molecule that regulates many aspects of human cell biology, and it is synthesized by enzymes known as poly(ADP-ribose) polymerases, or PARPs. A diverse collection of domain structures dictates the different cellular roles of PARP enzymes and regulates the production of poly(ADP-ribose). Here we primarily review recent structural insights into the regulation and catalysis of two family members: PARP-1 and Tankyrase. PARP-1 has multiple roles in the cellular response to DNA damage and the regulation of gene transcription, and Tankyrase regulates a diverse set of target proteins involved in cellular processes such as mitosis, genome integrity, and cell signaling. Both enzymes offer interesting modes of regulating the production and the target site selectivity of the poly(ADP-ribose) modification.

摘要

聚(ADP-核糖)是一种翻译后修饰和信号分子,调节着人类细胞生物学的许多方面,它由称为多聚(ADP-核糖)聚合酶或 PARP 的酶合成。多种结构域结构决定了 PARP 酶的不同细胞作用,并调节聚(ADP-核糖)的产生。在这里,我们主要综述了最近关于两个家族成员 PARP-1 和 Tankyrase 的调节和催化的结构见解。PARP-1 在细胞对 DNA 损伤的反应和基因转录的调节中具有多种作用,而 Tankyrase 调节着涉及有丝分裂、基因组完整性和细胞信号传导等细胞过程的一系列不同靶蛋白。这两种酶都提供了有趣的方式来调节聚(ADP-核糖)修饰的产生和靶位点选择性。

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The comings and goings of PARP-1 in response to DNA damage.PARP-1 在响应 DNA 损伤时的来来往往。
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Systems-wide Analysis of Serine ADP-Ribosylation Reveals Widespread Occurrence and Site-Specific Overlap with Phosphorylation.系统范围的丝氨酸 ADP-核糖基化分析揭示了广泛的发生和与磷酸化的特异性重叠。
DNA编码文库数据中广泛存在的假阴性:接头效应如何损害基于机器学习的先导化合物预测
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NUDT16 enhances the resistance of cancer cells to DNA-damaging agents by regulating replication fork stability via reversing HMGA1 ADP-ribosylation.NUDT16通过逆转HMGA1的ADP核糖基化来调节复制叉稳定性,从而增强癌细胞对DNA损伤剂的抗性。
J Biol Chem. 2025 Apr 25;301(6):108551. doi: 10.1016/j.jbc.2025.108551.
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FTO suppresses DNA repair by inhibiting PARP1.FTO通过抑制PARP1来抑制DNA修复。
Nat Commun. 2025 Mar 25;16(1):2925. doi: 10.1038/s41467-025-58309-0.
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