ReviewInternational journal of molecular sciences2025
Prime Editing in Dividing and Quiescent Cells.
Review in International journal of molecular sciences, 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.
- Article
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.
Funding
Abstract
Prime editing is a method of genome editing based on reverse transcription. Recent results have shown its elevated efficiency in dividing cells, which raises some questions regarding the mechanism of this effect, because prime editing does not employ homology-driven repair. This mini review aims to identify the reason for this phenomenon and find a possible solution to the problems that it poses. In dividing cells, prime editing takes advantage of high levels of dNTPs and active endonuclease and ligase machinery, such as FEN1 endonuclease and LIG1 ligase, but DNA mismatch repair, which is closely associated with replication, works against prime editing. Prime editing is a method which relies on retroviral reverse transcription, so mechanisms of intrinsic anti-retroviral defense should also work against editing. One of the factors which drastically reduce the efficiency of reverse translation is SAMHD1, which maintains low levels of dNTPs in non-dividing cells. Recent works aimed at the mitigation of SAMHD1 function demonstrated a significant increase in prime editing efficiency.
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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.