ArticleCell death discovery2025
Defects in DNA damage signaling and cell cycle checkpoints in a mouse model of Rhno1 deletion.
Article in Cell death discovery, 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
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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.
- A RHNO1-ATR/Chk1 positive feedback loop sustains the DNA replication stress response.bioRxiv : the preprint server for biology · 2026Article
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
In response to DNA damage or DNA replication stress, cells activate signaling pathways dependent on the kinase, ATR (Ataxia Telangiectasia and Rad3-Related). ATR signaling leads to induction of cell cycle checkpoints, a pause in DNA replication, and upregulation of DNA repair activities. In response to replication stress, ATR is activated by TOPBP1 (Topoisomerase II beta-Binding Protein 1) associated with the 9-1-1 (Rad9-Hus1-Rad1) complex. The three proteins that make up the 9-1-1 complex form a ring encircling DNA at damage sites and help localize TOPBP1 and ATR to signal the presence of damage or replication stress. RHNO1 (Rad9, Hus1, and Rad1-associated Nuclear Orphan 1) was identified as a protein that binds to components of the 9-1-1 complex to promote ATR signaling. Previous studies in cell lines have revealed that RHNO1 activity is required for maintenance of the G
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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 Socratic graph.