ReviewDNA repair2021
Collaborations between chromatin and nuclear architecture to optimize DNA repair fidelity.
Review in DNA repair, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed, 11 citations in OpenAlex.
- Overcoming natural replication barriers formed by DNA structures and the role of repositioning to the nuclear periphery.DNA repair · 2025Review
- Formation of chromosomal rearrangements inbioRxiv : the preprint server for biology · 2025Article
- A Novel Signature for Predicting Prognosis of Smoking-Related Squamous Cell Carcinoma.Frontiers in genetics · 2021Article
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
Homologous recombination (HR), considered the highest fidelity DNA double-strand break (DSB) repair pathway that a cell possesses, is capable of repairing multiple DSBs without altering genetic information. However, in "last resort" scenarios, HR can be directed to low fidelity subpathways which often use non-allelic donor templates. Such repair mechanisms are often highly mutagenic and can also yield chromosomal rearrangements and/or deletions. While the choice between HR and its less precise counterpart, non-homologous end joining (NHEJ), has received much attention, less is known about how cells manage and prioritize HR subpathways. In this review, we describe work focused on how chromatin and nuclear architecture orchestrate subpathway choice and repair template usage to maintain genome integrity without sacrificing cell survival. Understanding the relationships between nuclear architecture and recombination mechanics will be critical to understand these cellular repair decisions.
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.