ReviewFEBS letters2017
RecG controls DNA amplification at double-strand breaks and arrested replication forks.
Review in FEBS letters, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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
10 citing papers in PubMed, 20 citations in OpenAlex.
- Topoisomerase III limits RecA-dependent DNA amplification in the chromosome terminus with RecG.Nucleic acids research · 2026Article
- Rescuing the bacterial replisome at a nick requires recombinational repair and helicase reloading.Nature communications · 2025Article
- Biochemical and Structural Analyses Shed Light on the Mechanisms of RadD DNA Binding and Its ATPase fromInternational journal of molecular sciences · 2023Article
- Interplay between chromosomal architecture and termination of DNA replication in bacteria.Frontiers in microbiology · 2023Review
- Superfamily II helicases: the potential therapeutic target for cardiovascular diseases.Frontiers in cardiovascular medicine · 2023Review
- Movement of the RecG Motor Domain upon DNA Binding Is Required for Efficient Fork Reversal.International journal of molecular sciences · 2018Article
- Chromosomal over-replication in Escherichia coli recG cells is triggered by replication fork fusion and amplified if replichore symmetry is disturbed.Nucleic acids research · 2018Article
- Replication Fork Breakage and Restart in Escherichia coli.Microbiology and molecular biology reviews : MMBR · 2018Review
- Article
- Replication Restart in Bacteria.Journal of bacteriology · 2017Review
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
Abstract
DNA amplification is a powerful mutational mechanism that is a hallmark of cancer and drug resistance. It is therefore important to understand the fundamental pathways that cells employ to avoid over-replicating sections of their genomes. Recent studies demonstrate that, in the absence of RecG, DNA amplification is observed at sites of DNA double-strand break repair (DSBR) and of DNA replication arrest that are processed to generate double-strand ends. RecG also plays a role in stabilising joint molecules formed during DSBR. We propose that RecG prevents a previously unrecognised mechanism of DNA amplification that we call reverse-restart, which generates DNA double-strand ends from incorrect loading of the replicative helicase at D-loops formed by recombination, and at arrested replication forks.
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.