ArticleProceedings of the National Academy of Sciences of the United States of America1996
Activation of c-Jun N-terminal kinase in bacterial lipopolysaccharide-stimulated macrophages.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 128 papers.
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Who cites it
128 citing papers in PubMed, 470 citations in OpenAlex.
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- Resolvin D1 delivery to lesional macrophages using antioxidative black phosphorus nanosheets for atherosclerosis treatment.Nature nanotechnology · 2024Article
- Lysophosphatidylcholine Acetyltransferase 2 (Biology · 2024Article
- Valorization of coffee bean processing waste for the sustainable extraction of biologically active pectin.Heliyon · 2023Article
- The Impacts of Animal-Based Diets in Cardiovascular Disease Development: A Cellular and Physiological Overview.Journal of cardiovascular development and disease · 2023Review
- Mutations in the Vicinity of the IRAK3 Guanylate Cyclase Center Impact Its Subcellular Localization and Ability to Modulate Inflammatory Signaling in Immortalized Cell Lines.International journal of molecular sciences · 2023Article
- Rapid Profiling of Protein Complex Reorganization in Perturbed Systems.Journal of proteome research · 2023Article
- siRNA-MediatedInternational journal of molecular sciences · 2023Article
- Molecular Mechanisms Underlying the Anti-Inflammatory Properties of (R)-(-)-Carvone: Potential Roles of JNK1, Nrf2 and NF-κB.Pharmaceutics · 2023Article
- Macrophage-mediated tumor-targeted delivery of engineeredActa pharmaceutica Sinica. B · 2022Article
- FoxO3 might be involved in the inflammatory response of human monocytes to lipopolysaccharide through regulating expression of toll like receptor 4.Molecular biology reports · 2022Article
- Anti-Inflammatory Extract from Soil AlgaeCells · 2022Article
- The Effect of Natural-Based Formulation (NBF) on the Response of RAW264.7 Macrophages to LPS as an In Vitro Model of Inflammation.Journal of fungi (Basel, Switzerland) · 2022Article
- Taurodeoxycholic acid and valine reverse obesity-associated augmented alloimmune responses and prolong allograft survival.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2022Article
- A Newly Synthesized Flavone from Luteolin Escapes from COMT-Catalyzed Methylation and Inhibits Lipopolysaccharide-Induced Inflammation in RAW264.7 Macrophages via JNK, p38 and NF-κB Signaling Pathways.Journal of microbiology and biotechnology · 2022Article
- Coenzyme QOxidative medicine and cellular longevity · 2022Article
- Immunomodulatory Nanoparticles Mitigate Macrophage Inflammation via Inhibition of PAMP Interactions and Lactate-Mediated Functional Reprogramming of NF-κB and p38 MAPK.Pharmaceutics · 2021Article
- The Roles of c-Jun N-Terminal Kinase (JNK) in Infectious Diseases.International journal of molecular sciences · 2021Review
68 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Activation of macrophages by bacterial lipopolysaccharide (LPS) induces transcription of genes that encode for proinflammatory regulators of the immune response. Previous work has suggested that activation of the transcription factor activator protein 1 (AP-1) is one LPS-induced event that mediates this response. Consistent with this notion, we found that LPS stimulated AP-1-mediated transcription of a transfected reporter gene in the murine macrophage cell line RAW 264.7. As AP-1 activity is regulated in part by activation of the c-Jun N-terminal kinase (JNK), which phosphorylates and subsequently increases the transcriptional activity of c-Jun, we examined whether LPS treatment of macrophages resulted in activation of this kinase. LPS treatment of RAW 264.7 cells, murine bone marrow-derived macrophages, and the human monocyte cell line THP-1 resulted in rapid activation of the p46 and p54 isoforms of JNK. Treatment with wild-type and rough mutant forms of LPS and synthetic lipid A resulted in JNK activation, while pretreatment with the tyrosine kinase inhibitor herbimycin A inhibited this response. Binding of LPS-LPS binding protein (LBP) complexes to CD14, a surface receptor that mediates many LPS responses, was found to be crucial, as pretreatment of THP-1 cells with the monoclonal antibody 60b, which blocks this binding, inhibited JNK activation. These results suggest that LPS activation of JNK in monocyte/macrophage cells is a CD14- and protein tyrosine phosphorylation-dependent event that may mediate the early activation of AP-1 in regulating LPS-triggered gene induction.
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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.