Author

Christopher J. Staples

Bangor UniversityORCID 0000-0002-0482-9954Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Signature Assays, Organisms & Methods

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Approach:experimental assay· 3 Organism:human· 2 Research Focus:cell signaling & trafficking· 1 Research Focus:chromatin & epigenetic regulation· 1 Research Focus:development & morphogenesis· 1 Research Focus:host-pathogen & immune response· 1

Frequent Co-Authors

Amelia Gamble· 2 shared Caryl M Jones· 2 shared Daniel HarrisoniD· 2 shared Ellen G VernoniD· 2 shared Laura G. BennettiD· 2 shared Vithursha Thanendran· 2 shared Damiano Borrello· 1 shared Edgar HartsuikeriD· 1 shared

Activity by Year

2025-2026 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 41 mutual co-author links

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2 shared papersCancer Biology

Amelia Gamble

Mutual co-authors in cluster

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3 papers

Recent·Most cited

CIZ1 regulates G1 length and the CDK threshold for initiation of DNA replication to prevent DNA replication stress

James Tollitt, Marcus K Preedy, Tiernan Briggs, Sarah L. Allinson, Christopher J. Staples, Jason Luke Parsons, Richard L. Mort, Nikki A. Copeland

This study shows that CIZ1 regulates G1 length and the CDK threshold for DNA replication initiation, preventing DNA replication stress and genome instability.

Nucleic Acids Research · Sep 4, 2026Peer-reviewedCell Biology

IFI16 senses and protects stalled replication forks

Amelia Gamble, Thomas A. Ward, Otto P.G. Wheeler, Jessica P. Morris, Caryl M Jones, Laura G. Bennett, Ellen G Vernon, Vithursha Thanendran, Ilaria Ceppi, Swagata Halder, Damiano Borrello, Thomas D. J. Walker, Jahnavi Rajan, Hadil Suleiman, Daniel Harrison, , Christopher J. Staples

This paper shows that IFI16 detects stalled replication forks and triggers an innate immune response, while also protecting nascent DNA from degradation and aiding in fork protection in BRCA-deficient cells.

Molecular Cell · Jan 1, 2026Peer-reviewedCancer Biology

A nuclease-driven mechanism of post-replicative ssDNA gap suppression.

Laura G. Bennett, Vithursha Thanendran, Daniel Harrison, Caryl M Jones, Fay Antonopoulou, J Rajan, Ellen G Vernon, Amelia Gamble, Rolf Kraehenbuehl, Edgar Hartsuiker, Christopher J. Staples

This paper identifies a nuclease-driven mechanism for suppressing post-replicative ssDNA gaps, showing that MRNIP loss leads to MRE11-dependent gap filling via template switching.

bioRxiv · Oct 22, 2025 · PreprintCancer Biology