ReviewMolecular carcinogenesis2009
Checkpoint responses to unusual structures formed by DNA repeats.
Review in Molecular carcinogenesis, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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
29 citing papers in PubMed.
- Triplex H-DNA structure: the long and winding road from the discovery to its role in human disease.NAR molecular medicine · 2024Article
- Microsatellite break-induced replication generates highly mutagenized extrachromosomal circular DNAs.NAR cancer · 2024Article
- Pathogenic CANVAS (AAGGG)n repeats stall DNA replication due to the formation of alternative DNA structures.Nucleic acids research · 2024Article
- Rad9-mediated checkpoint activation is responsible for elevated expansions of GAA repeats in CST-deficient yeast.Genetics · 2021Article
- Replication stress at microsatellites causes DNA double-strand breaks and break-induced replication.The Journal of biological chemistry · 2020Article
- Short inverted repeats contribute to localized mutability in human somatic cells.Nucleic acids research · 2017Article
- Break-induced replication links microsatellite expansion to complex genome rearrangements.BioEssays : news and reviews in molecular, cellular and developmental biology · 2017Review
- Replication stalling and DNA microsatellite instability.Biophysical chemistry · 2017Review
- Centromeric DNA replication reconstitution reveals DNA loops and ATR checkpoint suppression.Nature cell biology · 2016Article
- The hidden side of unstable DNA repeats: Mutagenesis at a distance.DNA repair · 2015Review
- Regulation of recombination at yeast nuclear pores controls repair and triplet repeat stability.Genes & development · 2015Article
- The replicometer is broken: telomeres activate cellular senescence in response to genotoxic stresses.Aging cell · 2014Review
- Cis-acting DNA sequence at a replication origin promotes repeat expansion to fragile X full mutation.The Journal of cell biology · 2014Article
- Chromatin modifications and DNA repair: beyond double-strand breaks.Frontiers in genetics · 2014Review
- Timeless-dependent DNA replication-coupled recombination promotes Kaposi's Sarcoma-associated herpesvirus episome maintenance and terminal repeat stability.Journal of virology · 2013Article
- Oligodeoxynucleotide binding to (CTG) · (CAG) microsatellite repeats inhibits replication fork stalling, hairpin formation, and genome instability.Molecular and cellular biology · 2013Article
- Separation of intra-S checkpoint protein contributions to DNA replication fork protection and genomic stability in normal human fibroblasts.Cell cycle (Georgetown, Tex.) · 2013Article
- Inverted low-copy repeats and genome instability--a genome-wide analysis.Human mutation · 2013Article
- Local and global functions of Timeless and Tipin in replication fork protection.Cell cycle (Georgetown, Tex.) · 2012Review
- Replication fork stalling and checkpoint activation by a PKD1 locus mirror repeat polypurine-polypyrimidine (Pu-Py) tract.The Journal of biological chemistry · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
DNA sequences that are prone to adopting non-B DNA secondary structures are associated with hotspots of genomic instability. The fine mechanisms by which alternative DNA structures induce phenomena such as repeat expansions, chromosomal fragility, or gross chromosomal rearrangements are under intensive studies. It is well established that DNA damage checkpoint responses play a crucial role in maintaining a stable genome. It is far less clear, however, whether and how the checkpoint machinery responds to alternative DNA structures. This review discusses the role of the interplay between DNA damage checkpoints and alternative DNA structures in genome maintenance.
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.