ArticleThe Journal of biological chemistry2013
Nuclear factor-erythroid 2 (NF-E2) p45-related factor-2 (Nrf2) modulates dendritic cell immune function through regulation of p38 MAPK-cAMP-responsive element binding protein/activating transcription factor 1 signaling.
Article in The Journal of biological chemistry, 2013. 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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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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Who cites it
27 citing papers in PubMed, 53 citations in OpenAlex.
- Reactive oxygen species and metabolic checkpoints shape plasmacytoid dendritic cell fate in infection and autoimmunity.Redox biology · 2026Review
- Modulating ferroptosis sensitivity: environmental and cellular targets within the tumor microenvironment.Journal of experimental & clinical cancer research : CR · 2024Review
- Review
- Beyond Antioxidation: Keap1-Nrf2 in the Development and Effector Functions of Adaptive Immune Cells.ImmunoHorizons · 2023Review
- Emerging roles of activating transcription factor (ATF) family members in tumourigenesis and immunity: Implications in cancer immunotherapy.Genes & diseases · 2022Review
- Examination of Novel Immunomodulatory Effects of L-Sulforaphane.Nutrients · 2021Article
- Nrf2-A Molecular Target for Sepsis Patients in Critical Care.Biomolecules · 2020Review
- Loricrin: Past, Present, and Future.International journal of molecular sciences · 2020Review
- Potential Protective and Therapeutic Roles of the Nrf2 Pathway in Ocular Diseases: An Update.Oxidative medicine and cellular longevity · 2020Review
- Therapeutic targeting of the NRF2 and KEAP1 partnership in chronic diseases.Nature reviews. Drug discovery · 2019Review
- Emerging role of 12/15-Lipoxygenase (ALOX15) in human pathologies.Progress in lipid research · 2019Review
- Nrf2/ARE Pathway Modulation by Dietary Energy Regulation in Neurological Disorders.Frontiers in pharmacology · 2019Review
- Nrf2 Involvement in Chemical-Induced Skin Innate Immunity.Frontiers in immunology · 2019Review
- Article
- CD11c-Specific Deletion Reveals CREB as a Critical Regulator of DC Function during the Germinal Center Response.Journal of immunology research · 2018Article
- Oxidative Stress: Promoter of Allergic Sensitization to Protease Allergens?International journal of molecular sciences · 2017Review
- Role of Nuclear Factor (Erythroid-Derived 2)-Like 2 Signaling for Effects of Fumaric Acid Esters on Dendritic Cells.Frontiers in immunology · 2017Article
- Modulation of antigen processing by haem-oxygenase 1. Implications on inflammation and tolerance.Immunology · 2016Review
- Dimethyl fumarate blocks pro-inflammatory cytokine production via inhibition of TLR induced M1 and K63 ubiquitin chain formation.Scientific reports · 2016Article
- Crude Preparations of Helicobacter pylori Outer Membrane Vesicles Induce Upregulation of Heme Oxygenase-1 via Activating Akt-Nrf2 and mTOR-IκB Kinase-NF-κB Pathways in Dendritic Cells.Infection and immunity · 2016Article
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
Abstract
Nrf2 is a redox-responsive transcription factor that has been implicated in the regulation of DC immune function. Loss of Nrf2 results in increased co-stimulatory molecule expression, enhanced T cell stimulatory capacity, and increased reactive oxygen species (ROS) levels in murine immature DCs (iDCs). It is unknown whether altered immune function of Nrf2-deficient DCs (Nrf2(-/-) iDCs) is due to elevated ROS levels. Furthermore, it is unclear which intracellular signaling pathways are involved in Nrf2-mediated regulation of DC function. Using antioxidant vitamins to reset ROS levels in Nrf2(-/-) iDCs, we show that elevated ROS is not responsible for the altered phenotype and function of these DCs. Pharmacological inhibitors were used to explore the role of key MAPKs in mediating the altered phenotype and function in Nrf2(-/-) iDCs. We demonstrate that the increased co-stimulatory molecule expression (MHC II and CD86) and antigen-specific T cell activation capacity observed in Nrf2(-/-) iDCs was reversed by inhibition of p38 MAPK but not JNK. Importantly, we provide evidence for increased phosphorylation of cAMP-responsive element binding protein (CREB) and activating transcription factor 1 (ATF1), transcription factors that are downstream of p38 MAPK. The increased phosphorylation of CREB/ATF1 in Nrf2(-/-) iDCs was sensitive to p38 MAPK inhibition. We also show data to implicate heme oxygenase-1 as a potential molecular link between Nrf2 and CREB/ATF1. These results indicate that dysregulation of p38 MAPK-CREB/ATF1 signaling axis underlies the altered function and phenotype in Nrf2-deficient DCs. Our findings provide new insights into the mechanisms by which Nrf2 mediates regulation of DC function.
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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.