ArticleThe Journal of cell biology2002
Bloom's syndrome protein is required for correct relocalization of RAD50/MRE11/NBS1 complex after replication fork arrest.
Article in The Journal of cell biology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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Who cites it
55 citing papers in PubMed.
- DNA Damage Foci on Metaphase Chromosomes.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Review
- The CDK1-TOPBP1-PLK1 axis regulates the Bloom's syndrome helicase BLM to suppress crossover recombination in somatic cells.Science advances · 2022Article
- USP37 regulates DNA damage response through stabilizing and deubiquitinating BLM.Nucleic acids research · 2021Article
- A novel cell-cycle-regulated interaction of the Bloom syndrome helicase BLM with Mcm6 controls replication-linked processes.Nucleic acids research · 2021Article
- Hydroxyurea-The Good, the Bad and the Ugly.Genes · 2021Review
- Checkpoint functions of RecQ helicases at perturbed DNA replication fork.Current genetics · 2021Review
- MRE11-RAD50-NBS1 promotes Fanconi Anemia R-loop suppression at transcription-replication conflicts.Nature communications · 2019Article
- A new look at molecular biology of breast cancer.Cancer biology & therapy · 2019Review
- MRN complex-dependent recruitment of ubiquitylated BLM helicase to DSBs negatively regulates DNA repair pathways.Nature communications · 2018Article
- Article
- Quality control of homologous recombination.Cellular and molecular life sciences : CMLS · 2014Review
- On BLM helicase in recombination-mediated telomere maintenance.Molecular biology reports · 2013Article
- An N-terminal acidic region of Sgs1 interacts with Rpa70 and recruits Rad53 kinase to stalled forks.The EMBO journal · 2012Article
- Article
- RecQ helicases; at the crossroad of genome replication, repair, and recombination.Molecular biology reports · 2012Review
- Chromosome breakage is regulated by the interaction of the BLM helicase and topoisomerase IIalpha.Cancer research · 2011Article
- Time to bloom.Genome integrity · 2010Article
- Pathways of mammalian replication fork restart.Nature reviews. Molecular cell biology · 2010Review
- Unwinding protein complexes in ALTernative telomere maintenance.Journal of cellular biochemistry · 2010Review
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bloom's syndrome (BS) is a rare genetic disorder characterized by a broad range of symptoms and, most importantly, a predisposition to many types of cancers. Cells derived from patients with BS exhibit an elevated rate of somatic recombination and hypermutability, supporting a role for bleomycin (BLM) in the maintenance of genomic integrity. BLM is thought to participate in several DNA transactions, the failure of which could give raise to genomic instability, and to interact with many proteins involved in replication, recombination, and repair. In this study, we show that BLM function is specifically required to properly relocalize the RAD50/MRE11/NBS1 (RMN) complex at sites of replication arrest, but is not essential in the activation of BRCA1 either after stalled replication forks or gamma-rays. We also provide evidence that BLM is phosphorylated after replication arrest in an Ataxia and RAD3-related protein (ATR)-dependent manner and that phosphorylation is not required for subnuclear relocalization. Therefore, in ATR dominant negative mutant cells, the assembly of the RMN complex in nuclear foci after replication blockage is almost completely abolished. Together, these results suggest a relationship between BLM, ATR, and the RMN complex in the response to replication arrest, proposing a role for BLM protein and RMN complex in the resolution of stalled replication forks.
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