ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2011
The SUMO E3-ligase PIAS1 couples reactive oxygen species-dependent JNK activation to oxidative cell death.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 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, 58 citations in OpenAlex.
- ROS-SUMO Crosstalk in Oxidative Stress: Disease Mechanisms and Reproductive Health.Antioxidants (Basel, Switzerland) · 2026Review
- New Insights into TFEB SUMOylation and Its Role in Lipid Metabolism and Cardiovascular Disease.International journal of molecular sciences · 2025Review
- PIAS1/PIAS4-Mediated SUMOylation of TDP-43 Is Induced by Oxidative Stress.bioRxiv : the preprint server for biology · 2025Article
- Gene Regulatory Network Analysis of Decidual Stromal Cells and Natural Killer Cells.Reproductive sciences (Thousand Oaks, Calif.) · 2024Article
- Knocking Down PIAS3 Reduces HCell biochemistry and biophysics · 2024Article
- SUMOylation of Rho-associated protein kinase 2 induces goblet cell metaplasia in allergic airways.Nature communications · 2023Article
- Regulation of transforming growth factor-β signalling by SUMOylation and its role in fibrosis.Open biology · 2021Article
- The Formation of Melanocyte Apoptotic Bodies in Vitiligo and the Relocation of Vitiligo Autoantigens under Oxidative Stress.Oxidative medicine and cellular longevity · 2021Article
- The Role of Decidual Subpopulations in Implantation, Menstruation and Miscarriage.Frontiers in reproductive health · 2021Review
- The E3 Ligase PIAS1 Regulates p53 Sumoylation to Control Stress-Induced Apoptosis of Lens Epithelial Cells Through the Proapoptotic Regulator Bax.Frontiers in cell and developmental biology · 2021Article
- Protein inhibitor of activated STAT1 SerBritish journal of pharmacology · 2019Article
- Role of TG2-Mediated SERCA2 Serotonylation on Hypoxic Pulmonary Vein Remodeling.Frontiers in pharmacology · 2019Article
- Article
- Epigenetic regulation of HDAC1 SUMOylation as an endogenous neuroprotection against Aβ toxicity in a mouse model of Alzheimer's disease.Cell death and differentiation · 2017Article
- Progesterone-Dependent Induction of Phospholipase C-Related Catalytically Inactive Protein 1 (PRIP-1) in Decidualizing Human Endometrial Stromal Cells.Endocrinology · 2016Article
- Redox regulation of SUMO enzymes is required for ATM activity and survival in oxidative stress.The EMBO journal · 2016Article
- Article
- Hes-1 SUMOylation by protein inhibitor of activated STAT1 enhances the suppressing effect of Hes-1 on GADD45α expression to increase cell survival.Journal of biomedical science · 2014Article
- Sumoylation modulates oxidative stress relevant to the viability and functionality of pancreatic beta cells.American journal of translational research · 2014Review
- Possible involvement of CD10 in the development of endometriosis due to its inhibitory effects on CD44-dependent cell adhesion.Reproductive sciences (Thousand Oaks, Calif.) · 2014Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Human endometrial stromal cells (HESCs) exposed to reactive oxygen species (ROS) mount a hypersumoylation response in a c-Jun N-terminal kinase (JNK)-dependent manner. The mechanism that couples JNK signaling to the small ubiquitin-related modifier (SUMO) pathway and its functional consequences are not understood. We show that ROS-dependent JNK activation converges on the SUMO pathway via PIAS1 (protein inhibitor of activated STAT1). Unexpectedly, PIAS1 knockdown not only prevented ROS-dependent hypersumoylation but also enhanced JNK signaling in HESCs. Conversely, PIAS overexpression increased sumoylation of various substrates, including c-Jun, yet inhibited basal and ROS-dependent JNK activity independently of its SUMO ligase function. Expression profiling demonstrated that PIAS1 knockdown enhances and profoundly modifies the transcriptional response to oxidative stress signals. Using a cutoff of 2-fold change or more, a total of 250 ROS-sensitive genes were identified, 97 of which were not dependent on PIAS1. PIAS1 knockdown abolished the regulation of 43 genes but also sensitized 110 other genes to ROS. Importantly, PIAS1 silencing was obligatory for the induction of several cellular defense genes in response to oxidative stress. In agreement, PIAS1 knockdown attenuated ROS-dependent caspase-3/7 activation and subsequent apoptosis. Thus, PIAS1 determines the level of JNK activity in HESCs, couples ROS signaling to the SUMO pathway, and promotes oxidative cell death.
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