ArticleMethods in molecular biology (Clifton, N.J.)2023
Simultaneous Short- and Long-Patch Base Excision Repair (BER) Assay in Live Mammalian Cells.
Article in Methods in molecular biology (Clifton, N.J.), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed, 0 citations in OpenAlex.
- Article
- The relationship between DNA damage and repair and the occurrence and development of disease.Frontiers in genetics · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
The base excision repair (BER) pathway repairs small, non-bulky DNA lesions, including oxidized, alkylated, and deaminated bases, and is responsible for the removal of at least 20,000 DNA lesions per cell per day. BER is initiated by DNA damage-specific DNA glycosylases that excise the damaged base and generates an abasic (AP) site or single-strand breaks, which are subsequently repaired in mammalian cells either by single-nucleotide (SN) or multiple-nucleotide incorporation via the SN-BER or long-patch BER (LP-BER) pathway, respectively. This chapter describes a plaque-based host cell reactivation (PL-HCR) assay system for measuring BER mechanisms in live mammalian cells using a plasmid-based assay. After transfection of a phagemid (M13mp18) containing a single modified base (representative BER DNA substrates) within a restriction site into human cells, restriction digestions detect the presence or absence (complete repair) of the adduct by the transformation of the digestion products into E. coli and counting the transformants as plaques. To monitor the patch size, different plasmids are constructed containing C:A mismatches within different restriction sites (inhibiting digestion) at various distances on both sides (5' or 3') of the modified base-containing restriction sites. Using this assay, the percentage of repair events that occur via 5' and 3' patch formation can be quantified.
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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.