ReviewChromosoma2013
Regulation of telomere addition at DNA double-strand breaks.
Review in Chromosoma, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
21 citing papers in PubMed, 36 citations in OpenAlex.
- Neotelomeres and telomere-spanning chromosomal arm fusions in cancer genomes revealed by long-read sequencing.Cell genomics · 2024Article
- ATR blocks telomerase from converting DNA breaks into telomeres.Science (New York, N.Y.) · 2024Article
- Flexible Attachment and Detachment of Centromeres and Telomeres to and from Chromosomes.Biomolecules · 2023Review
- Chromothripsis as an on-target consequence of CRISPR-Cas9 genome editing.Nature genetics · 2021Article
- Article
- Mechanisms generating cancer genome complexity from a single cell division error.Science (New York, N.Y.) · 2020Article
- Biphasic recruitment of TRF2 to DNA damage sites promotes non-sister chromatid homologous recombination repair.Journal of cell science · 2018Article
- A Heterochromatin Domain Forms Gradually at a New Telomere and Is Dynamic at Stable Telomeres.Molecular and cellular biology · 2018Article
- Putting together and taking apart: assembly and disassembly of the Rad51 nucleoprotein filament in DNA repair and genome stability.Cell stress · 2018Review
- Article
- Cell cycle-dependent spatial segregation of telomerase from sites of DNA damage.The Journal of cell biology · 2017Article
- Derepression of hTERT gene expression promotes escape from oncogene-induced cellular senescence.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- RNA-template dependent de novo telomere addition.RNA biology · 2016Article
- Early Loss of Telomerase Action in Yeast Creates a Dependence on the DNA Damage Response Adaptor Proteins.Molecular and cellular biology · 2016Article
- Fragile sites of 45S rDNA of Lolium multiflorum are not hotspots for chromosomal breakages induced by X-ray.Molecular biology reports · 2016Article
- Dynamics of Human Telomerase Holoenzyme Assembly and Subunit Exchange across the Cell Cycle.The Journal of biological chemistry · 2015Article
- A transposable element within the Non-canonical telomerase RNA of Arabidopsis thaliana modulates telomerase in response to DNA damage [corrected].PLoS genetics · 2015Article
- Insertion of Retrotransposons at Chromosome Ends: Adaptive Response to Chromosome Maintenance.Frontiers in genetics · 2015Review
- Dna2 is involved in CA strand resection and nascent lagging strand completion at native yeast telomeres.The Journal of biological chemistry · 2013Article
- BRCA1 in the DNA damage response and at telomeres.Frontiers in genetics · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Telomeres constitute the ends of linear eukaryotic chromosomes. Due to the conventional mode of DNA replication, telomeric DNA erodes at each cell division. To counteract this, a specialized reverse transcriptase, telomerase, can elongate chromosome ends to maintain them at a constant average length. Because of their similarity to DNA double-strand breaks (DSBs), telomeres might be expected to induce a DNA damage response, which would lead to repair reactions and the generation of translocations or fusions. Many proteins present at telomeres prevent this by protecting (capping) the chromosome termini. Conversely, a DSB occurring in other regions of the genome, due, for instance, to a stalled replication fork or genotoxic agents, must be repaired by homologous recombination or end-joining to ensure genome stability. Interestingly, telomerase is able to generate a telomere de novo at an accidental DSB, with potentially lethal consequences in haploid cells and, at a minimum, loss of heterozygosity (LOH) in diploid cells. Recent data suggest that telomerase is systematically recruited to DSBs but is prevented from acting in the absence of a minimal stretch of flanking telomere-repeat sequences. In this review, we will focus on the mechanisms that regulate telomere addition to DSBs.
Indexed as
Identifiers
What OpenQuestion holds
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.