ArticleNature communications2015
Oscillation of p38 activity controls efficient pro-inflammatory gene expression.
Article in Nature communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 81 citations in OpenAlex.
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- Stress pathway outputs are encoded by pH-dependent clustering of kinase components.Nature communications · 2024Article
- Dynamical and combinatorial coding by MAPK p38 and NFκB in the inflammatory response of macrophages.Molecular systems biology · 2024Article
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- Fluorescence resonance energy transfer (FRET) spatiotemporal mapping of atypical P38 reveals an endosomal and cytosolic spatial bias.Scientific reports · 2023Article
- Hybrid Biophysics: Interdisciplinary approaches for trans-scale analysis of organism-environment interactions.Biophysics and physicobiology · 2023Article
- Computational modeling implicates protein scaffolding in p38 regulation of Akt.Journal of theoretical biology · 2022Article
- IDH2-mediated regulation of the biogenesis of the oxidative phosphorylation system.Science advances · 2022Article
- Genetically Encoded Fluorescent Biosensors for Biomedical Applications.Biomedicines · 2021Review
- Autonomous clocks that regulate organelle biogenesis, cytoskeletal organization, and intracellular dynamics.eLife · 2021Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The p38 MAP kinase signalling pathway controls inflammatory responses and is an important target of anti-inflammatory drugs. Although pro-inflammatory cytokines such as interleukin-1β (IL-1β) appear to induce only transient activation of p38 (over ∼ 60 min), longer cytokine exposure is necessary to induce p38-dependent effector genes. Here we study the dynamics of p38 activation in individual cells using a Förster resonance energy transfer (FRET)-based p38 activity reporter. We find that, after an initial burst of activity, p38 MAPK activity subsequently oscillates for more than 8 h under continuous IL-1β stimulation. However, as this oscillation is asynchronous, the measured p38 activity population average is only slightly higher than basal level. Mathematical modelling, which we have experimentally verified, indicates that the asynchronous oscillation of p38 is generated through a negative feedback loop involving the dual-specificity phosphatase MKP-1/DUSP1. We find that the oscillatory p38 activity is necessary for efficient expression of pro-inflammatory genes such as IL-6, IL-8 and COX-2.
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