ArticleThe Biochemical journal2001
Inhibitor of nuclear factor-kappaB induction by cAMP antagonizes interleukin-1-induced human macrophage-colony-stimulating-factor expression.
Article in The Biochemical journal, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 41 citations in OpenAlex.
- Dissecting PGENature communications · 2026Article
- The AMPK/cAMP Metabolic Signaling Axis as a Possible Therapeutic Target for Diabetes.Current molecular medicine · 2025Review
- Cyclic Adenosine Monophosphate in Cardiac and Sympathoadrenal GLP-1 Receptor Signaling: Focus on Anti-Inflammatory Effects.Pharmaceutics · 2024Review
- Cilostazol pretreatment prevents PTSD-related anxiety behavior through reduction of hippocampal neuroinflammation.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- Review
- NF-κB subunits direct kinetically distinct transcriptional cascades in antigen receptor-activated B cells.Nature immunology · 2023Article
- Endothelial Protein kinase D1 is a major regulator of post-traumatic hyperinflammation.Frontiers in immunology · 2023Article
- Emerging Role of cAMP/AMPK Signaling.Cells · 2022Review
- Major pathways involved in macrophage polarization in cancer.Frontiers in immunology · 2022Review
- Phosphodiesterase Inhibitors for Alzheimer's Disease: A Systematic Review of Clinical Trials and Epidemiology with a Mechanistic Rationale.Journal of Alzheimer's disease reports · 2020Review
- Phosphodiesterase-5 Inhibitors: Action on the Signaling Pathways of Neuroinflammation, Neurodegeneration, and Cognition.Mediators of inflammation · 2015Review
- Article
- Cyclic AMP: a selective modulator of NF-κB action.Cellular and molecular life sciences : CMLS · 2011Review
- Proinflammatory cytokines, IL-1β and TNF-α, induce expression of interleukin-34 mRNA via JNK- and p44/42 MAPK-NF-κB pathway but not p38 pathway in osteoblasts.Rheumatology international · 2011Article
- Cyclic AMP inhibits IL-1beta plus IFNgamma-induced NF-kappaB translocation in hepatocytes by a PKA independent mechanism.The Journal of surgical research · 2010Article
- Induction of IFN-beta and the innate antiviral response in myeloid cells occurs through an IPS-1-dependent signal that does not require IRF-3 and IRF-7.PLoS pathogens · 2009Article
- Oxidized {alpha}1-antitrypsin stimulates the release of monocyte chemotactic protein-1 from lung epithelial cells: potential role in emphysema.American journal of physiology. Lung cellular and molecular physiology · 2009Article
- The apolipoprotein E-mimetic peptide COG112 inhibits the inflammatory response to Citrobacter rodentium in colonic epithelial cells by preventing NF-kappaB activation.The Journal of biological chemistry · 2008Article
- Identification of N-(quinolin-8-yl)benzenesulfonamides as agents capable of down-regulating NFkappaB activity within two separate high-throughput screens of NFkappaB activation.Bioorganic & medicinal chemistry letters · 2008Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We have recently reported that interleukin-1alpha (IL-1alpha) can induce human macrophage colony-stimulating factor (M-CSF) expression through nuclear factor kappaB (NF-kappaB) activation, and treatment of human pancreatic MIA PaCa-2 cancer cells with forskolin or cAMP attenuated the NF-kappaB activation as well as M-CSF expression. In this study, we have further investigated the mechanism of cAMP attenuation. MIA PaCa-2 cells were incubated with forskolin or dibutyryl-cAMP and then stimulated with IL-1 for 1 h. Cell lysates were immunoprecipitated by anti-inhibitory kappaB (IkappaB) kinase-beta (IKKbeta) antibody and the immune complex assayed for kinase activity using recombinant inhibitor of NF-kappaB (IkappaBalpha) as substrate. The levels of IKKbeta in the respective cellular proteins were measured by subsequent Western blot. The results show that the level of IKK protein remains constant in the presence of cAMP, forskolin and/or IL-1, whereas IKK activity was robustly stimulated by IL-1. Nonetheless, dibutyryl-cAMP or forskolin did not affect the IKK activation induced by IL-1. This experiment suggests that elevated cAMP has no effect on IKK activity. IkappaBalpha protein level decreased markedly in IL-1-treated cells compared with the untreated. By contrast, cells treated with cAMP or forskolin possessed discernibly higher IkappaBalpha levels. In addition, we observed that forskolin potentiated and prolonged the IL-1-induced IkappaBalpha mRNA levels, whereas it did not stabilize the IkappaBalpha mRNA message. Wholly, these studies indicate that elevated cAMP antagonizes IL-1-induced M-CSF transcription by up-regulating IkappaBalpha gene induction and its consequent attenuation of NF-kappaB activation.
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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.