ArticleThe Journal of biological chemistry2014
Glycogen synthase kinase-3β stabilizes the interleukin (IL)-22 receptor from proteasomal degradation in murine lung epithelia.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 27 citations in OpenAlex.
- Acteoside relieves mesangial cell injury by regulating Th22 cell chemotaxis and proliferation in IgA nephropathy.Renal failure · 2018Trial
- Intrinsic renal cells induce lymphocytosis of Th22 cells from IgA nephropathy patients through B7-CTLA-4 and CCL-CCR pathways.Molecular and cellular biochemistry · 2018Trial
- Engineered outer membrane vesicle-like nanoparticles from Lactobacillus plantarum for oral IL-22 mRNA delivery and treatment of DSS-induced colitis.Molecular and cellular biochemistry · 2026Article
- Schizophrenia as a Disorder of Biological Barriers: A Narrative Review and Potential Interventions.International journal of molecular sciences · 2026Review
- Innate lymphoid cells in depression: Current status and perspectives.Biomarkers in neuropsychiatry · 2022Article
- Interleukin-22: a potential therapeutic target in atherosclerosis.Molecular medicine (Cambridge, Mass.) · 2021Review
- IL-37-induced activation of glycogen synthase kinase 3β promotes IL-1R8/Sigirr phosphorylation, internalization, and degradation in lung epithelial cells.Journal of cellular physiology · 2021Article
- GSK-3: a multifaceted player in acute leukemias.Leukemia · 2021Review
- Role of Th22 Cells in the Pathogenesis of Autoimmune Diseases.Frontiers in immunology · 2021Review
- IL-22 Plays a Critical Role in Maintaining Epithelial Integrity During Pulmonary Infection.Frontiers in immunology · 2020Review
- Nicotine Impairs the Response of Lung Epithelial Cells to IL-22.Mediators of inflammation · 2020Article
- Loss of adenomatous polyposis coli function renders intestinal epithelial cells resistant to the cytokine IL-22.PLoS biology · 2019Article
- The deubiquitinase USP13 stabilizes the anti-inflammatory receptor IL-1R8/Sigirr to suppress lung inflammation.EBioMedicine · 2019Article
- Differential Regulation of Type I and Type III Interferon Signaling.International journal of molecular sciences · 2019Review
- Phosphorylated E2F1 is stabilized by nuclear USP11 to drive Peg10 gene expression and activate lung epithelial cells.Journal of molecular cell biology · 2018Article
- Post-translational modification of the interferon-gamma receptor alters its stability and signaling.The Biochemical journal · 2017Article
- Insulin receptor substrate-1 deficiency drives a proinflammatory phenotype in KRAS mutant lung adenocarcinoma.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Attenuated Airway Epithelial Cell Interleukin-22R1 Expression in the Infant Nonhuman Primate Lung.American journal of respiratory cell and molecular biology · 2015Article
- The ubiquitin E3 ligase SCF-FBXO24 recognizes deacetylated nucleoside diphosphate kinase A to enhance its degradation.Molecular and cellular biology · 2015Article
- Fibrosis Related Inflammatory Mediators: Role of the IL-10 Cytokine Family.Mediators of inflammation · 2015Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Signaling through the interleukin (IL)-22 cytokine axis provides essential immune protection in the setting of extracellular infection as part of type 17 immunity. Molecular regulation of IL-22 receptor (IL-22R) protein levels is unknown. In murine lung epithelia, IL-22R is a relatively short-lived protein (t½ ∼1.5 h) degraded by the ubiquitin proteasome under normal unstimulated conditions, but its degradation is accelerated by IL-22 treatment. Lys(449) within the intracellular C-terminal domain of the IL-22R serves as a ubiquitin acceptor site as disruption of this site by deletion or site-directed mutagenesis creates an IL-22R variant that, when expressed in cells, is degradation-resistant and not ubiquitinated. Glycogen synthase kinase (GSK)-3β phosphorylates the IL-22R within a consensus phosphorylation signature at Ser(410) and Ser(414), and IL-22 treatment of cells triggers GSK-3β inactivation. GSK-3β overexpression results in accumulation of IL-22R protein, whereas GSK-3β depletion in cells reduces levels of the receptor. Mutagenesis of IL-22R at Ser(410) and Ser(414) results in receptor variants that display reduced phosphorylation levels and are more labile as compared with wild-type IL-22R when expressed in cells. Further, the cytoskeletal protein cortactin, which is important for epithelial spreading and barrier formation, is phosphorylated and activated at the epithelial cell leading edge after treatment with IL-22, but this effect is reduced after GSK-3β knockdown. These findings reveal the ability of GSK-3β to modulate IL-22R protein stability that might have significant implications for cytoprotective functions and therapeutic targeting of the IL-22 signaling axis.
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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.