ArticleNucleic acids research2003
Possible anti-recombinogenic role of Bloom's syndrome helicase in double-strand break processing.
Article in Nucleic acids research, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 21 citations in OpenAlex.
- Maladaptive somatic gene rescue as predisposition to JAK2 molecular abnormalities? Insights from an Israeli family.Annals of hematology · 2026Article
- Sex-specific differences in DNA double-strand break repair of cycling human lymphocytes during aging.Aging · 2021Article
- Role of the Exocyst Complex Component Sec6/8 in Genomic Stability.Molecular and cellular biology · 2015Article
- Depletion of the bloom syndrome helicase stimulates homology-dependent repair at double-strand breaks in human chromosomes.DNA repair · 2011Article
- Irradiated Blm-deficient mice are a highly tumor prone model for analysis of a broad spectrum of hematologic malignancies.Leukemia research · 2010Article
- Werner protein cooperates with the XRCC4-DNA ligase IV complex in end-processing.Biochemistry · 2008Article
- Cep164 is a mediator protein required for the maintenance of genomic stability through modulation of MDC1, RPA, and CHK1.Genes & development · 2008Article
- Phosphorylation of BLM, dissociation from topoisomerase IIIalpha, and colocalization with gamma-H2AX after topoisomerase I-induced replication damage.Molecular and cellular biology · 2005Article
- Recql5 and Blm RecQ DNA helicases have nonredundant roles in suppressing crossovers.Molecular and cellular biology · 2005Article
- Effects of camptothecin on double-strand break repair by non-homologous end-joining in DNA mismatch repair-deficient human colorectal cancer cell lines.Nucleic acids research · 2005Article
- Interplay between Drosophila Bloom's syndrome helicase and Ku autoantigen during nonhomologous end joining repair of P element-induced DNA breaks.Proceedings of the National Academy of Sciences of the United States of America · 2004Article
- Novel aspects of macromolecular repair and relationship to human disease.Journal of molecular medicine (Berlin, Germany) · 2004Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bloom's syndrome (BS) which associates genetic instability and predisposition to cancer is caused by mutations in the BLM gene encoding a RecQ family 3'-5' DNA helicase. It has been proposed that the generation of genetic instability in BS cells could result from an aberrant non-homologous DNA end joining (NHEJ), one of the two main DNA double-strand break (DSB) repair pathways in mammalian cells, the second major pathway being homologous recombination (HR). Using cell extracts, we report first that Ku70/80 and the catalytic subunit of the DNA-dependent protein kinase (DNA-PKcs), key factors of the end-joining machinery, and BLM are located in close proximity on DNA and that BLM binds to DNA only in the absence of ATP. In the presence of ATP, BLM is phosphorylated and dissociates from DNA in a strictly DNA-PKcs-dependent manner. We also show that BS cells display, in vivo, an accurate joining of DSBs, reflecting thus a functional NHEJ pathway. In sharp contrast, a 5-fold increase of the HR-mediated DNA DSB repair in BS cells was observed. These results support a model in which NHEJ activation mediates BLM dissociation from DNA, whereas, under conditions where HR is favored, e.g. at the replication fork, BLM exhibits an anti-recombinogenic role.
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