ArticlePloS one2011
Crosstalk between JNK and SUMO signaling pathways: deSUMOylation is protective against H2O2-induced cell injury.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 63 citations in OpenAlex.
- Article
- Modulation of Tau Pathology in Alzheimer's Disease by Dietary Bioactive Compounds.International journal of molecular sciences · 2024Review
- Regulation of transforming growth factor-β signalling by SUMOylation and its role in fibrosis.Open biology · 2021Article
- SUMOylation Regulates TDP-43 Splicing Activity and Nucleocytoplasmic Distribution.Molecular neurobiology · 2021Article
- Post-translational modification of RNA m6A demethylase ALKBH5 regulates ROS-induced DNA damage response.Nucleic acids research · 2021Article
- SUMO modification in apoptosis.Journal of molecular histology · 2021Review
- Regulation of ALS-Associated SOD1 Mutant SUMOylation and Aggregation by SENP and PIAS Family Proteins.Journal of molecular neuroscience : MN · 2020Article
- Fish c-Jun N-Terminal Kinase (JNK) Pathway Is Involved in Bacterial MDP-Induced Intestinal Inflammation.Frontiers in immunology · 2020Article
- Cellular Proteostasis in Neurodegeneration.Molecular neurobiology · 2019Review
- Role of TG2-Mediated SERCA2 Serotonylation on Hypoxic Pulmonary Vein Remodeling.Frontiers in pharmacology · 2019Article
- A post-translational balancing act: the good and the bad of SUMOylation in pancreatic islets.Diabetologia · 2018Article
- Targeting SUMO-1ylation Contrasts Synaptic Dysfunction in a Mouse Model of Alzheimer's Disease.Molecular neurobiology · 2017Review
- Battling Alzheimer's Disease: Targeting SUMOylation-Mediated Pathways.Neurochemical research · 2016Review
- CYLD and SUMO in neuroblastoma therapy.Oncoscience · 2016Article
- Protein Modifications as Manifestations of Hyperglycemic Glucotoxicity in Diabetes and Its Complications.Biochemistry insights · 2016Review
- Phosphorylation of Glutathione S-Transferase P1 (GSTP1) by Epidermal Growth Factor Receptor (EGFR) Promotes Formation of the GSTP1-c-Jun N-terminal kinase (JNK) Complex and Suppresses JNK Downstream Signaling and Apoptosis in Brain Tumor Cells.The Journal of biological chemistry · 2015Article
- Activation of Type 4 Metabotropic Glutamate Receptor Attenuates Oxidative Stress-Induced Death of Neural Stem Cells with Inhibition of JNK and p38 MAPK Signaling.Stem cells and development · 2015Article
- SUMO1 Affects Synaptic Function, Spine Density and Memory.Scientific reports · 2015Article
- High Phosphorylation Status of AKT/mTOR Signal in DESI2-Reduced Pancreatic Ductal Adenocarcinoma.Pathology oncology research : POR · 2015Article
- Presynaptic c-Jun N-terminal Kinase 2 regulates NMDA receptor-dependent glutamate release.Scientific reports · 2015Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundOxidative stress is a key feature in the pathogenesis of several neurological disorders. Following oxidative stress stimuli a wide range of pathways are activated and contribute to cellular death. The mechanism that couples c-Jun N-terminal kinase (JNK) signaling, a key pathway in stress conditions, to the small ubiquitin-related modifier (SUMO), an emerging protein in the field, is largely unknown. METHODOLOGY/PRINCIPAL
findingsWith this study we investigated if SUMOylation participates in the regulation of JNK activation as well as cellular death in a model of H(2)O(2) induced-oxidative stress. Our data show that H(2)O(2) modulates JNK activation and induces cellular death in neuroblastoma SH-SY5Y cells. Inhibition of JNK's action with the D-JNKI1 peptide rescued cells from death. Following H(2)O(2), SUMO-1 over-expression increased phosphorylation of JNK and exacerbated cell death, although only in conditions of mild oxidative stress. Furthermore inhibition of SUMOylation, following transfection with SENP1, interfered with JNK activation and rescued cells from H(2)O(2) induced death. Importantly, in our model, direct interaction between these proteins can occur. CONCLUSIONS/SIGNIFICANCE: Taken together our results show that SUMOylation may significantly contribute to modulation of JNK activation and contribute to cell death in oxidative stress conditions.
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