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Activating ATR, the devil's in the dETAA1l

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An Erratum to this article was published on 29 November 2016

This article has been updated

Two studies now show that Ewing's tumour-associated antigen 1 (ETAA1) is recruited to sites of DNA replication stress through its interaction with replication protein A, where it stimulates the ATR kinase to promote efficient genome duplication. These findings provide exciting insight into the already very complex regulatory mechanism of the ATR activation cascade.

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Figure 1: Model of ETAA1 recruitment to stressed replication forks.
Figure 2: A hypothetical model for the bimodal activation of ATR.

Change history

  • 04 November 2016

    In the version of this News and Views originally published, there was an error in Fig. 2: the protein 'TOPBP1' should have been in contact with the protein 'ATR'. This has been corrected in the online versions of the News and Views.

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  1. Wojciech Niedzwiedz is in the Department of Oncology, Weatherall Institute of Molecular Medicine, University of Oxford, Oxford, OX3 9DS, UK,

    Wojciech Niedzwiedz

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  1. Wojciech Niedzwiedz
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Correspondence to Wojciech Niedzwiedz.

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Niedzwiedz, W. Activating ATR, the devil's in the dETAA1l. Nat Cell Biol 18, 1120–1122 (2016). https://doi.org/10.1038/ncb3431

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