ArticleMedComm2022
SENP3-mediated TIP60 deSUMOylation is required for DNA-PKcs activity and DNA damage repair.
Article in MedComm, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 7 papers.
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
7 citing papers in PubMed, 11 citations in OpenAlex.
- GNL3 SUMOylation is essential for DNA double-strand break repair by homologous recombination.Nature communications · 2026Article
- Post-translational modifications of epigenetic modifier TIP60: their role in cellular functions and cancer.Epigenetics & chromatin · 2025Review
- The SUMO Family: Mechanisms and Implications in Thyroid Cancer Pathogenesis and Therapy.Biomedicines · 2024Review
- SENP5 promotes homologous recombination-mediated DNA damage repair in colorectal cancer cells through H2AZ deSUMOylation.Journal of experimental & clinical cancer research : CR · 2023Article
- Correction to: SENP3-mediated TIP60 deSUMOylation is required for DNA-PKcs activity and DNA damage repair.MedComm · 2022Article
- Cardiac-targeted PIASy gene silencing mediates deSUMOylation of caveolin-3 and prevents ischemia/reperfusion-induced NaMilitary Medical Research · 2022Article
- SENP3-mediated TIP60 deSUMOylation is required for DNA-PKcs activity and DNA damage repair.MedComm · 2022Article
Corrections and comments
- Erratum issued
- Retracted
Authors and funding
13 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The activation of DNA-dependent kinase (DNA-PKcs) upon DNA damage contains a cascade of reactions, covering acetylation by TIP60, binding with Ku70/80, and autophosphorylation. However, how cells regulate TIP60-mediated acetylation of DNA-PKcs and the following DNA-PKcs activation upon DNA damage remains obscure. This present study reported that TIP60 is hyper-SUMOylated in normal conditions, but upon irradiation-induced DNA damage, small ubiquitin-like modifier (SUMO)-specific protease 3 (SENP3)-mediated deSUMOylation of TIP60 promoted its interaction with DNA-PKcs to form the TIP60-DNA-PKcs complex. We show that TIP60 SUMOylation is reduced quickly in response to DNA damage and the deSUMOylation of TIP60 by SENP3 is required for DNA-PKcs acetylation and its autophosphorylation. Comet and γH2AX immunofluorescence assay showed that knockdown of SENP3 impaired DNA damage repair. Using the NHEJ report system, we found that knockdown of SENP3 affected the efficiency of NHEJ. Further exploration using clonogenic survival assay, cell viability assay and cytoflow assay suggested that leaking SENP3 increased the sensitivity of tumour cells to serval DNA damage treatment. Overall, our findings revealed a previously unidentified role of SENP3 in regulating DNA-PKcs activity and DNA damage repair.
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.