ArticleNucleic acids research2026
Nucleostemin promotes RAD51 filament assembly on double-stranded DNA to protect stalled replication forks.
Article in Nucleic acids research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
Abstract
Replication stress threatens genome integrity by stalling replication forks, which may lead to double-stranded DNA (dsDNA) breaks. Stalled replication forks can be rescued through the fork reversal mechanism, yet they remain vulnerable to nucleolytic attack. Here, we identify nucleostemin (NS/GNL3) as a critical fork-stabilizing factor. We show that NS rapidly accumulates at hydroxyurea-stalled forks and is indispensable for protecting reversed forks, with NS depletion abolishing RAD51 foci formation and unleashing MRE11-mediated degradation. Through biochemical reconstitution and single-molecule fluorescence resonance energy transfer (FRET), we demonstrate that NS binds DNA directly, engages RAD51, and promotes nucleoprotein filament assembly on the dsDNA segment adjacent to the single-stranded DNA/dsDNA junction. This NS-RAD51 complex synergistically shields nascent strands from MRE11-mediated nucleolytic attack. Our work uncovers a new mechanism of fork protection and positions NS as a key guardian of genome integrity under replication stress.
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.