ArticleMolecular and cellular biology1997
hMre11 and hRad50 nuclear foci are induced during the normal cellular response to DNA double-strand breaks.
Article in Molecular and cellular biology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 168 papers.
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Who cites it
168 citing papers in PubMed, 499 citations in OpenAlex.
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- PD-1/PD-L1 and DNA Damage Response in Cancer.Cells · 2023Review
- Adaptive Response in Rat Retinal Cell Cultures Irradiated with γ-rays.International journal of molecular sciences · 2023Article
- DNA Damage Foci on Metaphase Chromosomes.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Cancer and Radiosensitivity Syndromes: Is Impaired Nuclear ATM Kinase Activity the Primum Movens?Cancers · 2022Review
- Mre11-Rad50 oligomerization promotes DNA double-strand break repair.Nature communications · 2022Article
- A Proximity Ligation Method to Detect Proteins Bound to Single-Stranded DNA after DNA End Resection at DNA Double-Strand Breaks.Methods and protocols · 2021Article
- Mitochondrial cytochrome c shot towards histone chaperone condensates in the nucleus.FEBS open bio · 2021Review
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- Clinical significance of homologous recombination deficiency score testing in endometrial Cancer.Gynecologic oncology · 2021Article
- A framework for understanding the functions of biomolecular condensates across scales.Nature reviews. Molecular cell biology · 2021Review
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- Live Cell Imaging of Nuclear Actin Filaments and Heterochromatic Repair foci in Drosophila and Mouse Cells.Methods in molecular biology (Clifton, N.J.) · 2021Article
- Review
- The SNM1A DNA repair nuclease.DNA repair · 2020Review
- Modes of action of the archaeal Mre11/Rad50 DNA-repair complex revealed by fast-scan atomic force microscopy.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
108 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors at 1 institution in 2 countries.
Funding
Abstract
We previously identified a conserved multiprotein complex that includes hMre11 and hRad50. In this study, we used immunofluorescence to investigate the role of this complex in DNA double-strand break (DSB) repair. hMre11 and hRad50 form discrete nuclear foci in response to treatment with DSB-inducing agents but not in response to UV irradiation. hMre11 and hRad50 foci colocalize after treatment with ionizing radiation and are distinct from those of the DSB repair protein, hRad51. Our data indicate that an irradiated cell is competent to form either hMre11-hRad50 foci or hRad51 foci, but not both. The multiplicity of hMre11 and hRad50 foci is much higher in the DSB repair-deficient cell line 180BR than in repair-proficient cells. hMre11-hRad50 focus formation is markedly reduced in cells derived from ataxia-telangiectasia patients, whereas hRad51 focus formation is markedly increased. These experiments support genetic evidence from Saccharomyces cerevisiae indicating that Mre11-Rad50 have roles distinct from that of Rad51 in DSB repair. Further, these data indicate that hMre11-hRad50 foci form in response to DNA DSBs and are dependent upon a DNA damage-induced signaling pathway.
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Registered trials
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.