Roland Kanaar

This study identifies and characterizes P-motifs in BRCA2 and RAD54B that bind to DMC1 filaments through stable and transient interactions, revealing structural insights into their roles in meiotic recombination.

This study generates and characterizes induced pluripotent stem cell models with SMAD3 mutations to investigate LDS3 aneurysm formation mechanisms.

This study shows that FIGNL1 inhibits homologous recombination in BRCA2-deficient cells by preventing RAD51 filament removal, maintaining genome stability and viability.

This paper explains how BRCA2's FxxA and FxPP motifs bind to DMC1 and RAD51 via distinct interfaces, stabilizing recombinase filaments and explaining functional differences between these proteins.

This study investigates the functional impact of SMAD3 variants in patient-derived cells, showing distinct effects of dominant negative and haploinsufficient variants on disease manifestations and age of onset.

This paper investigates the role of BRCA2's meiotic domain in meiotic homologous recombination and proposes a model of chromosome pairing through tensed DNA tethers.

This paper identifies a cryptic BRCA2 repeated motif that binds to HSF2BP oligomers but does not affect meiotic recombination.

This study examines how BRCA2's DNA-binding and C-terminal domains affect its mobility and conformation during DNA repair, showing that C-terminal deletions do not significantly impact mobility but impair architectural changes and homologous recombination function.

The paper shows that low-dose ionizing radiation stimulates insertional mutagenesis in a γH2AX-dependent manner in human and mouse cells.

This study identifies HSF2BP as a regulator of homologous recombination in ICL repair by interacting with BRCA2, showing its role in genomic instability and cancer.