RAD18, WRNIP1 and ATMIN promote ATM signalling in response to replication stress View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2016-07

AUTHORS

Nnennaya Kanu, Tianyi Zhang, Rebecca A. Burrell, Atanu Chakraborty, Janet Cronshaw, Clive Da Costa, Eva Grönroos, Helen N. Pemberton, Emma Anderton, Laure Gonzalez, Simone Sabbioneda, Helle D. Ulrich, Charles Swanton, Axel Behrens

ABSTRACT

The DNA replication machinery invariably encounters obstacles that slow replication fork progression, and threaten to prevent complete replication and faithful segregation of sister chromatids. The resulting replication stress activates ATR, the major kinase involved in resolving impaired DNA replication. In addition, replication stress also activates the related kinase ATM, which is required to prevent mitotic segregation errors. However, the molecular mechanism of ATM activation by replication stress is not defined. Here, we show that monoubiquitinated Proliferating Cell Nuclear Antigen (PCNA), a marker of stalled replication forks, interacts with the ATM cofactor ATMIN via WRN-interacting protein 1 (WRNIP1). ATMIN, WRNIP1 and RAD18, the E3 ligase responsible for PCNA monoubiquitination, are specifically required for ATM signalling and 53BP1 focus formation induced by replication stress, not ionising radiation. Thus, WRNIP1 connects PCNA monoubiquitination with ATMIN/ATM to activate ATM signalling in response to replication stress and contribute to the maintenance of genomic stability. More... »

PAGES

4009

References to SciGraph publications

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/onc.2015.427

    DOI

    http://dx.doi.org/10.1038/onc.2015.427

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1053420394

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/26549024


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