ReviewEssays in biochemistry2025
DNA double strand break repair: a model of specificity and complexity in SUMO signalling.
Review in Essays in biochemistry, 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.
- SUMOylation of EphB4 enhances its stability in prostate cancer.British journal of cancer · 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
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Among the ubiquitin-like superfamily, small ubiquitin-like modifiers (SUMOs) are the most well-understood. However, in comparison with the prototypical small modifier ubiquitin, our understanding of the SUMO system lags. SUMOylation is often characterised as 'simple' in comparison with ubiquitination, with fewer SUMO-specific writers, readers and erasers compared with the ubiquitin machinery. A key divergence between ubiquitin and SUMO is that the SUMOylation system utilises a group of related SUMOs (SUMO1- 5), each possessing distinct functions. SUMO paralogs share conjugation, recognition and deconjugation machinery, yet signalling can employ each to perform specific cellular functions. This illustrates a complex layer of molecular discrimination that is far from simple. The repair of DNA double-stranded breaks (DSBs) - highly toxic DNA lesions generated from both endogenous and external sources - serves as a fascinating exemplar of specificity in SUMO signalling. This review focuses on how signalling specificity is achieved during SUMO-DSB repair. Examples of how different branches of SUMO signalling can direct discrete DSB-repair outcomes through modulation of key repair factors, including the RAP80-BRCA1-A complex, RNF168 and CtIP, are described in further detail.
Indexed as
Identifiers
What Socratic 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 Socratic graph.