This CIP2A tetramer has a dumbbell shape, with indirect DNA binding capacity at either end, through its binding-partner TOPBP1. This mechanistic insight explains its DNA tethering capacity in mitotic DNA repair.

Very pleased to share this new study: In a truly collaborative effort with the lab of Pim Huis in 't Veld @huis.bsky.social, we combined biochemistry with cell biological and genomic approaches to uncover how CIP2A works in mitotic DNA repair. www.biorxiv.org/content/10.6...

CIP2A tetramerization is required for mitotic DNA repair

DNA lesions that persist in mitosis threaten genome stability. These lesions recruit TOPBP1-CIP2A, a complex crucial to tether and process damaged DNA on mitotic chromosomes. Importantly, CIP2A is syn...

biorxiv.org

This study was spearheaded by talented PhD students Lauren de Haan @laurendehaan.bsky.social , and Rebecca Schneeweiss @rebeccaschneeweiss.bsky.social and supported by many labmembers and collaborators, including the labs of Jos Jonkers @josjonkers.bsky.social and Marcel Tijsterman.

We are holding our annual Rising Stars in Genetics and Genomics Postdoc Symposium on September 24-25, 2026! Please nominate postdocs who are conducting cutting edge, creative work, and are likely to be a leader in their field. Please nominate by April 30, 2026: forms.gle/85NZaxFezUk8... (1/2)

Extremely happy to share that my main PhD project about CIP2A-TOPBP1 and the SMX complex is now available online as pre-print. Huge thanks to all co-authors but especially @marcelvanvugt.bsky.social for giving me the opportunity to work on this exciting project! www.biorxiv.org/content/10.1...

CIP2A is required for mitotic recruitment of the SLX1/XPF/MUS81 tri-nuclease complex to replication stress-induced DNA lesions to maintain genome integrity

Perturbed DNA replication can lead to incompletely replicated DNA when cells enter mitosis and can interfere with chromosome segregation. Cells therefore require mechanisms to resolve these lesions du...

biorxiv.org

Happy to post a new study on BioRxiv, where we show Integrated Stress Response activation as an off-target effect of multiple clinically evaluated WEE1 inhibitors. Team effort with the lab of Dan Durocher @durocher1.bsky.social and many others. www.biorxiv.org/content/10.1...

WEE1 inhibitors trigger GCN2-mediated activation of the integrated stress response

The WEE1 kinase negatively regulates CDK1/2 to control DNA replication and mitotic entry. Genetic factors that determine sensitivity to WEE1 inhibitors (WEE1i) are largely unknown. A genome-wide inser...

biorxiv.org

Thank you to Roger Greenberg and Hilda Pickett for organising a fantastic 2025 Mammalian DNA Repair GRC in Ventura, California. Looking forward to the next time.

Happy to share our study by Francien Talens and many colleagues on RAD51 foci formation as a functional marker for PARPi sensitivity in ovarian cancer PDX models. academic.oup.com/narcancer/ar...

RAD51 recruitment but not replication fork stability associates with PARP inhibitor response in ovarian cancer patient-derived xenograft models

Abstract. Poly(ADP‐ribose) polymerase (PARP) inhibitors (PARPis) are currently used to treat BRCA1/2 mutant cancers. Although PARPi sensitivity has been at

academic.oup.com