ReviewFrontiers in physiology2020
The Critical Roles of the SUMO-Specific Protease SENP3 in Human Diseases and Clinical Implications.
Review in Frontiers in physiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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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.
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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.
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Who cites it
18 citing papers in PubMed, 29 citations in OpenAlex.
- Sentrin-specific protease 3 (SENP3)-mediated Krüppel-like factor 4 (KLF4) deSUMOylation regulates vascular smooth muscle cell phenotypic switching in atherosclerosis.Molecular biomedicine · 2025Article
- PELP1 coordinates the modular assembly and enzymatic activity of the rixosome complex.Science advances · 2025Article
- Exploring ID4 as a driver of aggression and a therapeutic target in triple-negative breast cancer.NPJ breast cancer · 2025Article
- SENP3 Drives Abdominal Aortic Aneurysm Development by Regulating Ferroptosis via De-SUMOylation of CTH.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Regulation of mitochondrial dynamics in cardiomyocytes: implications for cardiac health and disease.Frontiers in cell and developmental biology · 2025Review
- Editorial: Post-translational modifications in human cancer: pharmacological insights and therapeutic opportunities.Frontiers in pharmacology · 2025Article
- SENP3 Promotes Mantle Cell Lymphoma Development through Regulating Wnt10a Expression.Current medical science · 2024Article
- Distinctive tumorigenic significance and innovative oncology targets of SUMOylation.Theranostics · 2024Review
- Circular RNA MAP2K2-modified immunosuppressive dendritic cells for preventing alloimmune rejection in organ transplantation.Bioengineering & translational medicine · 2024Article
- Brucella effectors NyxA and NyxB target SENP3 to modulate the subcellular localisation of nucleolar proteins.Nature communications · 2023Article
- SENP3 Aggravates Renal Tubular Epithelial Cell Apoptosis in Lipopolysaccharide-Induced Acute Kidney Injury via deSUMOylation of Drp1.Kidney diseases (Basel, Switzerland) · 2022Article
- Article
- Cancer-Associated Dysregulation of Sumo Regulators: Proteases and Ligases.International journal of molecular sciences · 2022Review
- SENP3-mediated TIP60 deSUMOylation is required for DNA-PKcs activity and DNA damage repair.MedComm · 2022Article
- Hypoxia-induced NFATc3 deSUMOylation enhances pancreatic carcinoma progression.Cell death & disease · 2022Article
- EAPB0503, an Imidazoquinoxaline Derivative Modulates SENP3/ARF Mediated SUMOylation, and Induces NPM1c Degradation in NPM1 Mutant AML.International journal of molecular sciences · 2022Article
- A Capra hircus chromosome 19 locus linked to milk production influences mammary conformation.Journal of animal science and biotechnology · 2022Article
- SENP3 promotes tumor progression and is a novel prognostic biomarker in triple-negative breast cancer.Frontiers in oncology · 2022Article
Corrections and comments
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Post-translational modification by SUMO (small ubiquitin-like modifier) proteins has been shown to regulate a variety of functions of proteins, including protein stability, chromatin organization, transcription, DNA repair, subcellular localization, protein-protein interactions, and protein homeostasis. SENP (sentrin/SUMO-specific protease) regulates precursor processing and deconjugation of SUMO to control cellular mechanisms. SENP3, which is one of the SENP family members, deconjugates target proteins to alter protein modification. The effect of modification via SUMO and SENP3 is crucial to maintain the balance of SUMOylation and guarantee normal protein function and cellular activities. SENP3 acts as an oxidative stress-responsive molecule under physiological conditions. Under pathological conditions, if the SUMOylation process of proteins is affected by variations in SENP3 levels, it will cause a cellular reaction and ultimately lead to abnormal cellular activities and the occurrence and development of human diseases, including cardiovascular diseases, neurological diseases, and various cancers. In this review, we summarized the most recent advances concerning the critical roles of SENP3 in normal physiological and pathological conditions as well as the potential clinical implications in various diseases. Targeting SENP3 alone or in combination with current therapies might provide powerful targeted therapeutic strategies for the treatment of these diseases.
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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.