ArticleCytogenetic and genome research2008
Loss of homologous recombination or non-homologous end-joining leads to radial formation following DNA interstrand crosslink damage.
Article in Cytogenetic and genome research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 24 citations in OpenAlex.
- The tight bond between Fanconi anemia and aging.Frontiers in aging · 2026Review
- Fanconi anemia-associated chromosomal radial formation is dependent on POLθ-mediated alternative end joining.Cell reports · 2023Article
- The Combination of Panobinostat and Melphalan for the Treatment of Patients with Multiple Myeloma.International journal of molecular sciences · 2022Article
- Mitotic Antipairing of Homologous Chromosomes.Results and problems in cell differentiation · 2022Article
- DNA Double-Strand Breaks Affect Chromosomal Rearrangements during Methotrexate-Mediated Gene Amplification in Chinese Hamster Ovary Cells.Pharmaceutics · 2021Article
- Review
- The FANC/BRCA Pathway Releases Replication Blockades by Eliminating DNA Interstrand Cross-Links.Genes · 2020Review
- DNA polymerase ζ limits chromosomal damage and promotes cell survival following aflatoxin exposure.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Article
- BRCA2 is needed for both repair and cell cycle arrest in mammalian cells exposed to S23906, an anticancer monofunctional DNA binder.Cell cycle (Georgetown, Tex.) · 2015Article
- Bloom syndrome radials are predominantly non-homologous and are suppressed by phosphorylated BLM.Cytogenetic and genome research · 2014Article
- Advances in understanding the complex mechanisms of DNA interstrand cross-link repair.Cold Spring Harbor perspectives in biology · 2013Review
- Fanconi anemia (FA) binding protein FAAP20 stabilizes FA complementation group A (FANCA) and participates in interstrand cross-link repair.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Embryonic lethality after combined inactivation of Fancd2 and Mlh1 in mice.Cancer research · 2009Article
- DNA interstrand crosslink repair in mammalian cells.Journal of cellular physiology · 2009Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
High levels of interstrand cross-link damage in mammalian cells cause chromatid breaks and radial formations recognizable by cytogenetic examination. The mechanism of radial formation observed following DNA damage has yet to be determined. Due to recent findings linking homologous recombination and non-homologous end-joining to the action of the Fanconi anemia pathway, we speculated that radials might be the result of defects in either of the pathways of DNA repair. To test this hypothesis, we have investigated the role of homologous recombination proteins RAD51 and RAD52, non-homologous end-joining proteins Ku70 and LIG4, and protein MRE11 in radial formation and cell survival following interstrand crosslink damage with mitomycin C. For the studies we used small inhibitory RNA to deplete the proteins from cells, allowing for evaluation of radial formation and cell survival. In transformed normal human fibroblasts, depletion of these proteins increased interstrand crosslink sensitivity as manifested by decreased cell survival and increased radial formation. These results demonstrate that inactivation of proteins from either of the two separate DNA repair pathways increases cellular sensitivity to interstrand crosslinks, indicating each pathway plays a role in the normal response to interstrand crosslink damage. We can also conclude that homologous recombination or non-homologous end-joining are not required for radial formation, since radials occur with depletion of these pathways.
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