ArticleMolecular and cellular biology2003
Retention but not recruitment of Crb2 at double-strand breaks requires Rad1 and Rad3 complexes.
Article in Molecular and cellular biology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
63 citing papers in PubMed, 95 citations in OpenAlex.
- Homologous recombination suppresses transgenerational DNA end resection and chromosomal instability in fission yeast.Nucleic acids research · 2023Article
- Aberrant association of chromatin with nuclear periphery induced by Rif1 leads to mitotic defect.Life science alliance · 2023Article
- Repair Kinetics of DSB-Foci Induced by Proton and α-Particle Microbeams of Different Energies.Life (Basel, Switzerland) · 2022Article
- Article
- Fission yeast Ase1Molecular biology research communications · 2021Article
- Review
- An Assay to Study Intra-Chromosomal Deletions in Yeast.Methods and protocols · 2019Article
- XPG-related nucleases are hierarchically recruited for double-stranded rDNA break resection.The Journal of biological chemistry · 2019Article
- The NuA4 acetyltransferase and histone H4 acetylation promote replication recovery after topoisomerase I-poisoning.Epigenetics & chromatin · 2019Article
- Tdp1 processes chromate-induced single-strand DNA breaks that collapse replication forks.PLoS genetics · 2018Article
- Lingering single-strand breaks trigger Rad51-independent homology-directed repair of collapsed replication forks in the polynucleotide kinase/phosphatase mutant of fission yeast.PLoS genetics · 2017Article
- Meiotic chromosome mobility in fission yeast is resistant to environmental stress.Scientific reports · 2016Article
- Acentric chromosome ends are prone to fusion with functional chromosome ends through a homology-directed rearrangement.Nucleic acids research · 2016Article
- Ku stabilizes replication forks in the absence of Brc1.PloS one · 2015Article
- Increased meiotic crossovers and reduced genome stability in absence of Schizosaccharomyces pombe Rad16 (XPF).Genetics · 2014Article
- Brc1 links replication stress response and centromere function.Cell cycle (Georgetown, Tex.) · 2013Review
- Mapping genomic hotspots of DNA damage by a single-strand-DNA-compatible and strand-specific ChIP-seq method.Genome research · 2013Article
- Mre11 ATLD17/18 mutation retains Tel1/ATM activity but blocks DNA double-strand break repair.Nucleic acids research · 2012Article
- Replication fork collapse and genome instability in a deoxycytidylate deaminase mutant.Molecular and cellular biology · 2012Article
- A new method to efficiently induce a site-specific double-strand break in the fission yeast Schizosaccharomyces pombe.Yeast (Chichester, England) · 2012Article
3 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The fission yeast checkpoint protein Crb2, related to budding yeast Rad9 and human 53BP1 and BRCA1, has been suggested to act as an adapter protein facilitating the phosphorylation of specific substrates by Rad3-Rad26 kinase. To further understand its role in checkpoint signaling, we examined its localization in live cells by using fluorescence microscopy. In response to DNA damage, Crb2 localizes to distinct nuclear foci, which represent sites of DNA double-strand breaks (DSBs). Crb2 colocalizes with Rad22 at persistent foci, suggesting that Crb2 is retained at sites of DNA damage during repair. Damage-induced Crb2 foci still form in cells defective in Rad1, Rad3, and Rad17 complexes, but these foci do not persist as long as in wild-type cells. Our results suggest that Crb2 functions at the sites of DNA damage, and its regulated persistent localization at damage sites may be involved in facilitating DNA repair and/or maintaining the checkpoint arrest while DNA repair is under way.
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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.