• Publications
  • Influence
Targeting the DNA repair defect in BRCA mutant cells as a therapeutic strategy
TLDR
BRCA1 or BRCA2 dysfunction unexpectedly and profoundly sensitizes cells to the inhibition of PARP enzymatic activity, resulting in chromosomal instability, cell cycle arrest and subsequent apoptosis, illustrating how different pathways cooperate to repair damage. Expand
The Bloom's syndrome helicase suppresses crossing over during homologous recombination
TLDR
It is shown that mutations in BLM and hTOPO IIIα together effect the resolution of a recombination intermediate containing a double Holliday junction and prevents exchange of flanking sequences, which has wider implications for the understanding of the process of homologous recombination and the mechanisms that exist to prevent tumorigenesis. Expand
XRCC1 coordinates the initial and late stages of DNA abasic site repair through protein–protein interactions
TLDR
It is reported here that XRCC1, another essential protein involved in the maintenance of genome stability, physically interacts with APE1 and stimulates its enzymatic activities, extending the coordinating role of XR CC1 to the initial step of the repair of DNA abasic sites. Expand
Replication stress induces sister-chromatid bridging at fragile site loci in mitosis
TLDR
It is shown that the Fanconi anaemia proteins FANCD2 and FANCI specifically associate with common fragile site loci irrespective of whether the chromosome is broken, and this work proposes that, after replication stress, sister chromatids are interlinked by replication intermediates primarily at genetic loci with intrinsic replication difficulties, such as fragile sites. Expand
BLM is required for faithful chromosome segregation and its localization defines a class of ultrafine anaphase bridges
TLDR
It is proposed that sister‐chromatid disjunction is often incomplete in human cells even after the onset of anaphase, and a model for the action of BLM is presented in ensuring complete sister chromatid decatenation in anaphases. Expand
RecQ helicases: caretakers of the genome
  • I. Hickson
  • Biology, Medicine
  • Nature Reviews Cancer
  • 1 March 2003
TLDR
RecQ helicases are highly conserved from bacteria to man and seem to maintain genomic stability by functioning at the interface between DNA replication and DNA repair. Expand
53BP1 nuclear bodies form around DNA lesions generated by mitotic transmission of chromosomes under replication stress
TLDR
It is shown that mild replication stress increases the frequency of chromosomal lesions that are transmitted to daughter cells, and evidence is provided that 53BP1 nuclear bodies shield chromosomal fragile sites sequestered in these compartments against erosion. Expand
The structure-specific endonuclease Mus81 contributes to replication restart by generating double-strand DNA breaks
TLDR
It is suggested that Mus81 suppresses chromosomal instability by converting potentially detrimental replication-associated DNA structures into intermediates that are more amenable to DNA repair. Expand
The Bloom’s Syndrome Helicase Unwinds G4 DNA*
TLDR
G4 DNA is a preferred substrate of the BLM helicase, as measured both by efficiency of unwinding and by competition, which suggests that G4 DNA may be a natural substrate of BLM in vivo and that the failure to unwind G4DNA may cause the genomic instability and increased frequency of sister chromatid exchange characteristic of Bloom’s syndrome. Expand
Telomere-binding Protein TRF2 Binds to and Stimulates the Werner and Bloom Syndrome Helicases*
TLDR
In human cells, it is reported that WRN co-localizes and physically interacts with the critical telomere maintenance protein TRF2, and this interaction is mediated by the RecQ conserved C-terminal region of WRN. Expand
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