Publications by authors named "B J M van Kooij"
Article Synopsis
- During DNA repair, some types of damage cause breaks in the DNA, and a special group called the Fanconi anemia (FA) core complex helps fix these breaks.
- Researchers found that two members of this complex, FANCL and Ube2T, play an important role in fixing DNA breaks even when they aren't caused by interstrand crosslinks (ICLs).
- The study showed that FANCL helps gather other repair proteins at the break sites, making it easier for the cell to fix the DNA properly.
Metal-Mediated Synthesis of a Mixed Arduengo-Fischer Carbodicarbene Ligand.
Angew Chem Int Ed Engl
August 2024
Carbodicarbenes are strong C-donor ligands, which have found numerous applications in organometallic and main group element chemistry. Herein, we report a structurally distinct carbodicarbene ligand, which is formed by dinitrogenative coupling of a Fischer carbene complex with an N-heterocyclic diazoolefin. The resulting carbonyl complex serves as a stable source for the mixed Arduengo-Fischer carbodicarbene ligand.
View Article and Find Full Text PDFArticle Synopsis
- - Overexpression of Cyclin E1 disrupts DNA replication, leading to DNA damage and instability, which forces cancer cells to rely on repair mechanisms like RAD52-mediated break-induced replication.
- - Many DNA lesions caused by Cyclin E1 during the S phase are not repaired before mitosis, resulting in mitotic DNA synthesis (MiDAS) that depends on RAD52.
- - Targeting RAD52 during mitosis can reduce the viability of Cyclin E1-overexpressing cells, and a positive link between Cyclin E1 amplification and RAD52 levels is found in breast cancer samples, highlighting RAD52’s role in maintaining genomic stability.
Article Synopsis
- When BRCA1 and BRCA2 genes are mutated, they can't fix DNA breaks properly, which can lead to cancer.
- Scientists found that cells with BRCA1 mutations rely on a factor called EXO1 to fix DNA damage, making EXO1 a weak spot for these cells.
- If EXO1 is missing in BRCA1-mutated cells, they struggle to repair DNA breaks, but BRCA2-mutated cells can still manage without EXO1, suggesting that targeting EXO1 could help treat BRCA1-related cancers.
Article Synopsis
- Homologous Recombination (HR) is a precise mechanism that repairs DNA Double-Strand Breaks (DSBs), which can occur due to various damaging factors like radiation or chemicals.
- The study identified members of the Fanconi anemia (FA) core complex, specifically FANCL and Ube2T, as key players in promoting HR at DSBs, even independent of interstrand crosslinks (ICLs).
- The findings also highlight that FANCL's activity is crucial for recruiting the nuclease CtIP to DSB sites, which is necessary for effective HR, suggesting a dual role for the FA complex in DNA repair.