ReviewDNA repair2025
Targeting DNA damage sensors for cancer therapy.
Review in DNA repair, 2025. 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.
- Evaluation of the total antioxidant capacity of Anchusa italica retz using carbon fiber microelectrode modified by Au-Ag alloy urchin-like nanostructures.Mikrochimica acta · 2025Article
- BKScientific reports · 2025Article
- The Multifaceted Role of Rad9 in the DNA Damage Response of Saccharomyces cerevisiae.Yeast (Chichester, England)Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
DNA damage occurs from both endogenous and exogenous sources and DNA damaging agents are a mainstay in cancer therapeutics. DNA damage sensors (DDS) are proteins that recognize and bind to unique DNA structures that arise from direct DNA damage or replication stress and are the first step in the DNA damage response (DDR). DNA damage sensors are responsible for recruiting transducer proteins that signal downstream DNA repair pathways. As the initiating proteins, DDS are excellent candidates for anti-cancer drug targeting to limit DDR activation. Here, we review four major DDS: PARP1, RPA, Ku, and the MRN complex. We briefly describe the cellular DDS functions before analyzing the structural mechanisms of DNA damage sensing. Lastly, we examine the current state of the field towards inhibiting each DDS for anti-cancer therapeutics and broadly discuss the therapeutic potential for DDS targeting.
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.