ArticleNucleic acids research2004
A Rad50-dependent pathway of DNA repair is deficient in Fanconi anemia fibroblasts.
Article in Nucleic acids research, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 18 citations in OpenAlex.
- The FANC/BRCA Pathway Releases Replication Blockades by Eliminating DNA Interstrand Cross-Links.Genes · 2020Review
- Dysfunctional DNA repair pathway via defective FANCD2 gene engenders multifarious exomic and transcriptomic effects in Fanconi anemia.Molecular genetics & genomic medicine · 2018Article
- The MRE11 complex: starting from the ends.Nature reviews. Molecular cell biology · 2011Review
- Cellular and molecular consequences of defective Fanconi anemia proteins in replication-coupled DNA repair: mechanistic insights.Mutation research · 2009Review
- Transcriptome-guided characterization of genomic rearrangements in a breast cancer cell line.Proceedings of the National Academy of Sciences of the United States of America · 2009Article
- Defective signal joint recombination in fanconi anemia fibroblasts reveals a role for Rad50 in V(D)J recombination.Journal of molecular biology · 2007Article
- Disparate contributions of the Fanconi anemia pathway and homologous recombination in preventing spontaneous mutagenesis.Nucleic acids research · 2007Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Fanconi anemia (FA) is a fatal genetic disorder associated with pancytopenia and cancer. Cells lacking functional FA genes are hypersensitive to bifunctional alkylating agents, and are deficient in DNA double-strand break repair. Multiple genes with FA-causing mutations have been cloned, however, the molecular basis for FA remains obscure. The results presented herein indicate that a Rad50-dependent end-joining process is non-functional in diploid fibroblasts from FA patients. Introduction of anti-Rad50 antibody into normal fibroblasts sensitized them to DNA damaging agents, whereas this treatment had no effect on fibroblasts from FA patients. The DNA end-joining process deficient in FA cells also requires the Mre11, Nbs1 and DNA ligase IV proteins. These data reveal the existence of a previously uncharacterized Rad50-dependent DNA double-strand break repair pathway in mammalian somatic cells, and suggest that failure to activate this pathway is responsible, at least in part, for the defective DNA end-joining observed in FA cells.
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