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核小体重塑ATP酶ISWI受多聚ADP核糖基化调控。

The nucleosome-remodeling ATPase ISWI is regulated by poly-ADP-ribosylation.

作者信息

Sala Anna, La Rocca Gaspare, Burgio Giosalba, Kotova Elena, Di Gesù Dario, Collesano Marianna, Ingrassia Antonia M R, Tulin Alexei V, Corona Davide F V

机构信息

Istituto Telethon Dulbecco, Universita' degli Studi di Palermo, Palermo, Italy.

出版信息

PLoS Biol. 2008 Oct 14;6(10):e252. doi: 10.1371/journal.pbio.0060252.

DOI:10.1371/journal.pbio.0060252
PMID:18922045
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2567001/
Abstract

ATP-dependent nucleosome-remodeling enzymes and covalent modifiers of chromatin set the functional state of chromatin. However, how these enzymatic activities are coordinated in the nucleus is largely unknown. We found that the evolutionary conserved nucleosome-remodeling ATPase ISWI and the poly-ADP-ribose polymerase PARP genetically interact. We present evidence showing that ISWI is target of poly-ADP-ribosylation. Poly-ADP-ribosylation counteracts ISWI function in vitro and in vivo. Our work suggests that ISWI is a physiological target of PARP and that poly-ADP-ribosylation can be a new, important post-translational modification regulating the activity of ATP-dependent nucleosome remodelers.

摘要

ATP 依赖的核小体重塑酶和染色质的共价修饰剂决定了染色质的功能状态。然而,这些酶活性在细胞核中是如何协调的,目前很大程度上尚不清楚。我们发现,进化上保守的核小体重塑 ATP 酶 ISWI 与聚 ADP 核糖聚合酶 PARP 在遗传上相互作用。我们提供的证据表明,ISWI 是聚 ADP 核糖基化的靶点。聚 ADP 核糖基化在体外和体内都能对抗 ISWI 的功能。我们的研究表明,ISWI 是 PARP 的生理靶点,并且聚 ADP 核糖基化可能是一种新的、重要的翻译后修饰,可调节 ATP 依赖的核小体重塑酶的活性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa9a/2573926/f061e9558926/pbio.0060252.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa9a/2573926/fdd19f9f5398/pbio.0060252.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa9a/2573926/f061e9558926/pbio.0060252.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa9a/2573926/fdd19f9f5398/pbio.0060252.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa9a/2573926/f061e9558926/pbio.0060252.g003.jpg

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