ArticlePLoS genetics2014
Disruption of SUMO-specific protease 2 induces mitochondria mediated neurodegeneration.
Article in PLoS genetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 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.
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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
45 citing papers in PubMed, 76 citations in OpenAlex.
- Organelle regulation of SUMOylation: regulatory mechanisms and therapeutic application.Journal of advanced research · 2026Review
- Stem cell-associated osteogenic deficiency causes craniofacial deformities with progeroid accumulation of prelamin A.JCI insight · 2026Article
- Role of vascular smooth muscle phenotypic transformation induced by histone modifications in the development of abdominal aortic aneurysms.Clinical epigenetics · 2025Review
- Astragaloside IV combined with ligustrazine ameliorates abnormal mitochondrial dynamics via Drp1 SUMO/deSUMOylation in cerebral ischemia-reperfusion injury.CNS neuroscience & therapeutics · 2024Article
- The PML hub: An emerging actor of leukemia therapies.The Journal of experimental medicine · 2023Article
- miRNA-27a is essential for bone remodeling by modulating p62-mediated osteoclast signaling.eLife · 2023Article
- Possible molecular mechanisms underlying the development of atherosclerosis in cancer survivors.Frontiers in cardiovascular medicine · 2023Review
- Discovery of a Dual SENP1 and SENP2 Inhibitor.International journal of molecular sciences · 2022Article
- SUMOylation and Major Depressive Disorder.International journal of molecular sciences · 2022Review
- SENP2 regulates mitochondrial function and insulin secretion in pancreatic β cells.Experimental & molecular medicine · 2022Article
- Protein sumoylation in normal and cancer stem cells.Frontiers in molecular biosciences · 2022Review
- Identification of Natural Products as SENP2 Inhibitors for Targeted Therapy in Heart Failure.Frontiers in pharmacology · 2022Article
- Natural Products Against Renal FibrosisFrontiers in pharmacology · 2022Review
- SUMOylation modification-mediated cell death.Open biology · 2021Review
- Inhibition of Drp1 SUMOylation by ALR protects the liver from ischemia-reperfusion injury.Cell death and differentiation · 2021Article
- BMPR1A maintains skeletal stem cell properties in craniofacial development and craniosynostosis.Science translational medicine · 2021Article
- SUMO-specific Isopeptidases Tuning Cardiac SUMOylation in Health and Disease.Frontiers in molecular biosciences · 2021Review
- SUMOylation as a Therapeutic Target for Myocardial Infarction.Frontiers in cardiovascular medicine · 2021Review
- The role of SUMOylation during development.Biochemical Society transactions · 2020Review
- Forebrain excitatory neuron-specific SENP2 knockout mouse displays hyperactivity, impaired learning and memory, and anxiolytic-like behavior.Molecular brain · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Post-translational modification of proteins by small ubiquitin-related modifier (SUMO) is reversible and highly evolutionarily conserved from yeasts to humans. Unlike ubiquitination with a well-established role in protein degradation, sumoylation may alter protein function, activity, stability and subcellular localization. Members of SUMO-specific protease (SENP) family, capable of SUMO removal, are involved in the reversed conjugation process. Although SUMO-specific proteases are known to reverse sumoylation in many well-defined systems, their importance in mammalian development and pathogenesis remains largely elusive. In patients with neurodegenerative diseases, aberrant accumulation of SUMO-conjugated proteins has been widely described. Several aggregation-prone proteins modulated by SUMO have been implicated in neurodegeneration, but there is no evidence supporting a direct involvement of SUMO modification enzymes in human diseases. Here we show that mice with neural-specific disruption of SENP2 develop movement difficulties which ultimately results in paralysis. The disruption induces neurodegeneration where mitochondrial dynamics is dysregulated. SENP2 regulates Drp1 sumoylation and stability critical for mitochondrial morphogenesis in an isoform-specific manner. Although dispensable for development of neural cell types, this regulatory mechanism is necessary for their survival. Our findings provide a causal link of SUMO modification enzymes to apoptosis of neural cells, suggesting a new pathogenic mechanism for neurodegeneration. Exploring the protective effect of SENP2 on neuronal cell death may uncover important preventive and therapeutic strategies for neurodegenerative 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 OpenQuestion graph.