ArticleScience advances2025
Endogenous p21 levels protect genomic stability by suppressing both excess and restrained nascent DNA syntheses.
Article in Science advances, 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.
- Evaluation of non-canonical p53 functions in DNA replication and recombination for variant classification.Cell death & disease · 2026Article
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
No grant is acknowledged in the PubMed record.
Abstract
The rate of DNA synthesis is crucial for full DNA duplication. We report a key role of p21 in controlling this rate. During normal replication, p21 promotes nascent DNA synthesis alongside the DNA polymerase iota (Pol ι)/p53 complex. When p21 is down-regulated but detectable, nascent DNA tracks are longer and discontinuous and rely on primase and DNA polymerase (PrimPol). With the complete elimination of p21, nascent DNA tracks become shorter and continuous and depend on Pol kappa (κ). Endogenous p21 levels are critical for genomic stability, as both PrimPol- and Pol κ-mediated syntheses can induce chromosomal instability. The residual expression of p21 in p53-null cells influences the involvement of PrimPol or Pol κ in nascent DNA synthesis and subsequent chromosomal instability. Our results demonstrate that endogenous levels of p21 in cycling cells, insufficient for cyclin-dependent kinase inhibition, prevent genomic instability through proliferating cell nuclear antigen binding (PCNA), limiting PrimPol and Pol κ's role in nascent DNA synthesis.
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.