ArticleCells2012
Multiple strategies for translesion synthesis in bacteria.
Article in Cells, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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
11 citing papers in PubMed, 29 citations in OpenAlex.
- Investigating the composition and recruitment of the mycobacterial ImuA'-ImuB-DnaE2 mutasome.eLife · 2023Article
- Mechanistic insight into the repair of C8-linked pyrrolobenzodiazepine monomer-mediated DNA damage.RSC medicinal chemistry · 2022Article
- Coexistence of SOS-Dependent and SOS-Independent Regulation of DNA Repair Genes in Radiation-ResistantCells · 2021Review
- Pseudouridines of tRNA Anticodon Stem-Loop Have Unexpected Role in Mutagenesis inMicroorganisms · 2020Article
- Visualizing mutagenic repair: novel insights into bacterial translesion synthesis.FEMS microbiology reviews · 2020Review
- Article
- Article
- Contribution of increased mutagenesis to the evolution of pollutants-degrading indigenous bacteria.PloS one · 2017Article
- Replisome-mediated translesion synthesis and leading strand template lesion skipping are competing bypass mechanisms.The Journal of biological chemistry · 2014Article
- Transient hypermutagenesis accelerates the evolution of legume endosymbionts following horizontal gene transfer.PLoS biology · 2014Article
- DNA polymerase IV mediates efficient and quick recovery of replication forks stalled at N2-dG adducts.Nucleic acids research · 2014Article
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 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Damage to DNA is common and can arise from numerous environmental and endogenous sources. In response to ubiquitous DNA damage, Y-family DNA polymerases are induced by the SOS response and are capable of bypassing DNA lesions. In Escherichia coli, these Y-family polymerases are DinB and UmuC, whose activities are modulated by their interaction with the polymerase manager protein UmuD. Many, but not all, bacteria utilize DinB and UmuC homologs. Recently, a C-family polymerase named ImuC, which is similar in primary structure to the replicative DNA polymerase DnaE, was found to be able to copy damaged DNA and either carry out or suppress mutagenesis. ImuC is often found with proteins ImuA and ImuB, the latter of which is similar to Y‑family polymerases, but seems to lack the catalytic residues necessary for polymerase activity. This imuAimuBimuC mutagenesis cassette represents a widespread alternative strategy for translesion synthesis and mutagenesis in bacteria. Bacterial Y‑family and ImuC DNA polymerases contribute to replication past DNA damage and the acquisition of antibiotic resistance.
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.