ArticleProceedings of the National Academy of Sciences of the United States of America2003
The human Bloom syndrome gene suppresses the DNA replication and repair defects of yeast dna2 mutants.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 66 citations in OpenAlex.
- Review
- Review
- Multiple roles of DNA2 nuclease/helicase in DNA metabolism, genome stability and human diseases.Nucleic acids research · 2020Review
- An enhanced CRISPR repressor for targeted mammalian gene regulation.Nature methods · 2018Article
- Dna2 initiates resection at clean DNA double-strand breaks.Nucleic acids research · 2017Article
- Abro1 maintains genome stability and limits replication stress by protecting replication fork stability.Genes & development · 2017Article
- Interacting partners of FEN1 and its role in the development of anticancer therapeutics.Oncotarget · 2017Review
- Nucleolytic processing of aberrant replication intermediates by an Exo1-Dna2-Sae2 axis counteracts fork collapse-driven chromosome instability.Nucleic acids research · 2016Article
- A Selective Small Molecule DNA2 Inhibitor for Sensitization of Human Cancer Cells to Chemotherapy.EBioMedicine · 2016Article
- Wuho Is a New Member in Maintaining Genome Stability through its Interaction with Flap Endonuclease 1.PLoS biology · 2016Article
- A Dominant Mutation in Human RAD51 Reveals Its Function in DNA Interstrand Crosslink Repair Independent of Homologous Recombination.Molecular cell · 2015Article
- MCM8-9 complex promotes resection of double-strand break ends by MRE11-RAD50-NBS1 complex.Nature communications · 2015Article
- Borrowing nuclear DNA helicases to protect mitochondrial DNA.International journal of molecular sciences · 2015Review
- RecQ helicase and RecJ nuclease provide complementary functions to resect DNA for homologous recombination.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- The DNA2 nuclease/helicase is an estrogen-dependent gene mutated in breast and ovarian cancers.Oncotarget · 2014Article
- Preventing over-resection by DNA2 helicase/nuclease suppresses repair defects in Fanconi anemia cells.Cell cycle (Georgetown, Tex.) · 2014Article
- The MCM8-MCM9 complex promotes RAD51 recruitment at DNA damage sites to facilitate homologous recombination.Molecular and cellular biology · 2013Article
- Human Fanconi anemia complementation group a protein stimulates the 5' flap endonuclease activity of FEN1.PloS one · 2013Article
- Flap endonuclease 1.Annual review of biochemistry · 2013Review
- Okazaki fragment processing-independent role for human Dna2 enzyme during DNA replication.The Journal of biological chemistry · 2012Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Bloom syndrome is a disorder of profound and early cancer predisposition in which cells become hypermutable, exhibit high frequency of sister chromatid exchanges, and show increased micronuclei. BLM, the gene mutated in Bloom syndrome, has been cloned previously, and the BLM protein is a member of the RecQ family of DNA helicases. Many lines of evidence suggest that BLM is involved either directly in DNA replication or in surveillance during DNA replication, but its specific roles remain unknown. Here we show that hBLM can suppress both the temperature-sensitive growth defect and the DNA damage sensitivity of the yeast DNA replication mutant dna2-1. The dna2-1 mutant is defective in a helicase-nuclease that is required either to coordinate with the crucial Saccharomyces cerevisiae (sc) FEN1 nuclease in Okazaki fragment maturation or to compensate for scFEN1 when its activity is impaired. We show that human BLM interacts with both scDna2 and scFEN1 by using coimmunoprecipitation from yeast extracts, suggesting that human BLM participates in the same steps of DNA replication or repair as scFEN1 and scDna2.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.