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Antony Oliver on Muck Rack

Antony Oliver

Delaware
As seen in: LinkedIn, Nature, BioRxiv, Cell Press, The Architects' Journal, New Civil Engineer, BIM+
Dr Antony W. Oliver - Genome Damage and Stability Centre, School of Life Sciences, University of Sussex, UK; pronouns: he/him opinions: his own
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Articles

Break-induced replication is enhanced by a phospho-activated RPA-binding module in Pol32

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By David Jones, Rowin Appanah, Luke Yates, Antony Oliver, Ulrich Rass
| Nature Verified
Abstract Break-induced replication (BIR) facilitates single-ended DNA double-strand break (DSB) repair. Upon homologous recombination-mediated strand invasion into a homologous repair template, BIR is catalysed by a minimal replisome comprising PCNA, DNA polymerase δ (Pol δ), and the Pif1 helicase. Here, we identify an interaction between Pol δ and single-stranded DNA (ssDNA)-binding protein RPA mediated by an RPA-binding module (RBM) within Pol δ subunit Pol32 and RPA subunit Rfa1.
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The CIP2A-TOPBP1 axis facilitates mitotic DNA repair via MiDAS and MMEJ - Nature Communications

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By Peter Martin, Jadwiga Nieminuszczy, Karen Lane, Jörg Mansfeld, Antony Oliver, Jessica A. Downs, Jyoti Choudhary, Matthew Day, Maxime Lecot
| Nature Verified
Abstract Mitotic DNA double-strand breaks (DSBs) accumulate in response to replication stress or BRCA1/2 deficiency posing a significant threat to genome stability as repair by non-homologous end-joining (NHEJ) and homologous recombination (HR) is largely inactivated in mitosis. Instead, mitotic cells rely on alternative repair processes such as microhomology-mediated end-joining (MMEJ) and mitotic DNA synthesis (MiDAS).
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The balance between B55α and Greatwall expression levels predicts sensitivity to Greatwall inhibition in cancer cells - Nature Communications

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By Robert Zach, Sandra M. Martín-Guerrero, Abdulrahman A. Alatawi, Kim Hou Chia, Alex Herbert, Ryan West, john spencer, Thomas Hunt, David Andrews, Pedro R. Cutillas, Antony Oliver, Simon Ward Verified
| Nature Verified
Abstract The Greatwall kinase inhibits PP2A-B55 phosphatase activity during mitosis to stabilise critical Cdk1-driven mitotic phosphorylation. Although Greatwall represents a potential oncogene and prospective therapeutic target, our understanding of the cellular and molecular consequences of chemical Greatwall inactivation remains limited.
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