ReviewPhilosophical transactions of the Royal Society of London. Series B, Biological sciences2017
SUMO, a small, but powerful, regulator of double-strand break repair.
Review in Philosophical transactions of the Royal Society of London. Series B, Biological sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 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
46 citing papers in PubMed, 79 citations in OpenAlex.
- Protein Posttranslational Modifications in Immunity: Molecular Mechanisms and Therapeutic Targets.MedComm · 2026Review
- Systematic discovery of UFM1 receptors reveals a regulatory module in DNA repair directing non-homologous end-joining.Nature communications · 2026Article
- Exon-skipping antisense oligonucleotides targeting SUMO1 and SUMO2 demonstrate chemosensitizing effects in NSCLC cells in tissue culture.Research square · 2026Article
- DNA double strand break repair: a model of specificity and complexity in SUMO signalling.Essays in biochemistry · 2025Review
- HDAC6-dependent deacetylation of SAE2 enhances SUMO1 conjugation for mitotic integrity.The EMBO journal · 2025Article
- Conversion of Ku80 K568 crotonylation to SUMOylation facilitates DNA non-homologous end joining and cancer radioresistance.Signal transduction and targeted therapy · 2025Article
- PIN1-SUMO2/3 motif suppresses excessive RNF168 chromatin accumulation and ubiquitin signaling to promote IR resistance.Nature communications · 2025Article
- Solo or in Concert: SUMOylation in Pathogenic Fungi.The plant pathology journal · 2025Review
- SUMO and the DNA damage response.Biochemical Society transactions · 2024Review
- SUMOylation of Bonus, theeLife · 2023Article
- SENP6 regulates localization and nuclear condensation of DNA damage response proteins by group deSUMOylation.Nature communications · 2023Article
- Comprehensive Interactome Mapping of the DNA Repair Scaffold SLX4 Using Proximity Labeling and Affinity Purification.Journal of proteome research · 2023Article
- SUMO monoclonal antibodies vary in sensitivity, specificity, and ability to detect types of SUMO conjugate.Scientific reports · 2022Article
- Stress combined with loss of the Candida albicans SUMO protease Ulp2 triggers selection of aneuploidy via a two-step process.PLoS genetics · 2022Article
- SENP3-mediated TIP60 deSUMOylation is required for DNA-PKcs activity and DNA damage repair.MedComm · 2022Article
- Microarray screening reveals two non-conventional SUMO-binding modules linked to DNA repair by non-homologous end-joining.Nucleic acids research · 2022Article
- ZMYM2 restricts 53BP1 at DNA double-strand breaks to favor BRCA1 loading and homologous recombination.Nucleic acids research · 2022Article
- The Next Frontier: Translational Development of Ubiquitination, SUMOylation, and NEDDylation in Cancer.International journal of molecular sciences · 2022Review
- SUMOylation regulates the number and size of promyelocytic leukemia-nuclear bodies (PML-NBs) and arsenic perturbs SUMO dynamics on PML by insolubilizing PML in THP-1 cells.Archives of toxicology · 2022Article
- Regulation of SUMOylation Targets Associated With Wnt/β-Catenin Pathway.Frontiers in oncology · 2022Review
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 at 1 institution in 2 countries.
Funding
Abstract
The response to a DNA double-stranded break in mammalian cells is a process of sensing and signalling the lesion. It results in halting the cell cycle and local transcription and in the mediation of the DNA repair process itself. The response is launched through a series of post-translational modification signalling events coordinated by phosphorylation and ubiquitination. More recently modifications of proteins by
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.