ArticleNucleic acids research2025
Pathways and products of base excision DNA repair in Xenopus laevis eggs: contrast with human cell pathways.
Article in Nucleic acids research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- 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
5 authors.
Funding
Abstract
Endogenous DNA damage is mutagenic and cytotoxic unless removed by base excision DNA repair (BER). BER replaces 2-10 nucleotides in "long patch" (LP-BER) or just one nucleotide in the simpler "short-patch" SP-BER. LP-BER is required for some oxidative lesions. Xenopus laevis egg extracts (HSS) had robust BER of diverse lesions (uracil and various abasic sites). It was surprising to find no evidence for HSS repair of 8-oxoguanine, an important mutagenic lesion. Also unexpected was the independence of HSS BER from DNA polymerase β (Polβ), which typically contributes both DNA repair synthesis and 5' "trimming" to SP-BER. Instead, HSS BER was blocked by aphidicolin inhibiting the replication DNA polymerases δ and ε. Added human Polβ restored full repair, requiring only its 5'-trimming activity, not its DNA polymerase function. Mass-labeled probes revealed that Xenopus BER repair patches were 80%-90% 2-nucleotide (2-nt) LP-BER tracts. Supplementing the low Polβ level in HSS with recombinant enzyme shifted BER toward 1-nt (SP-BER) patches, also influenced by the surrounding sequence. Excision upstream (5') of the lesion occurred in most of the frog BER products. In contrast, human cell (HEK293) extracts had Polβ-dependent BER, with mostly 2-nt repair patches. Human LP-BER was driven by the Fen1 flap endonuclease, but it did not include 5' excision.
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.