ArticleMolecular systems biology2011
Tristetraprolin-driven regulatory circuit controls quality and timing of mRNA decay in inflammation.
Article in Molecular systems biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.
What it found
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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
76 citing papers in PubMed, 109 citations in OpenAlex.
- The ZFP36 Family as a Post-Transcriptional Immune Checkpoint in Immunity and Disease: Molecular Mechanisms and Functional Implications.Biomolecules · 2026Review
- Tristetraprolin protects against ozone-induced acute lung injury and inflammation in mice.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- Functional interplay between TTP/ZFP36 and HuR/ELAVL1 in cancer: a post-transcriptional regulatory network.Frontiers in oncology · 2026Review
- Restraint of inflammasome-driven cytokine responses through the mRNA stability protein TTP.Cell reports · 2025Article
- ZFP36 Regulates Vascular Smooth Muscle Contraction and Maintains Blood Pressure.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- RNA-binding proteins in cardiovascular biology and disease: the beat goes on.Nature reviews. Cardiology · 2024Review
- The mRNA-Binding Protein KSRP Limits the Inflammatory Response of Macrophages.International journal of molecular sciences · 2024Article
- Synergistic roles of tristetraprolin family members in myeloid cells in the control of inflammation.Life science alliance · 2024Article
- HUWE1 controls tristetraprolin proteasomal degradation by regulating its phosphorylation.eLife · 2023Article
- Variability of the innate immune response is globally constrained by transcriptional bursting.Frontiers in molecular biosciences · 2023Article
- Stress signaling boosts interferon-induced gene transcription in macrophages.Science signaling · 2022Article
- Multiomics analysis couples mRNA turnover and translational control of glutamine metabolism to the differentiation of the activated CD4Scientific reports · 2022Article
- Clinical implications of tristetraprolin (TTP) modulation in the treatment of inflammatory diseases.Pharmacology & therapeutics · 2022Review
- TTP-mediated regulation of mRNA stability in immune cells contributes to adaptive immunity, immune tolerance and clinical applications.RNA biology · 2021Review
- Aberrant Post-Transcriptional Regulation of Protein Expression in the Development of Chronic Obstructive Pulmonary Disease.International journal of molecular sciences · 2021Review
- Article
- Review
- The RNA-binding protein tristetraprolin regulates RALDH2 expression by intestinal dendritic cells and controls local Treg homeostasis.Mucosal immunology · 2021Article
- Conceptual Advances in Control of Inflammation by the RNA-Binding Protein Tristetraprolin.Frontiers in immunology · 2021Review
- P23 Acts as Functional RBP in the Macrophage Inflammation Response.Frontiers in molecular biosciences · 2021Article
16 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
For a successful yet controlled immune response, cells need to specifically destabilize inflammatory mRNAs but prevent premature removal of those still used. The regulatory circuits controlling quality and timing in the global inflammatory mRNA decay are not understood. Here, we show that the mRNA-destabilizing function of the AU-rich element-binding protein tristetraprolin (TTP) is inversely regulated by the p38 MAPK activity profile such that after inflammatory stimulus the TTP-dependent decay is initially limited to few mRNAs. With time, the TTP-dependent decay gradually spreads resulting in cumulative elimination of one third of inflammation-induced unstable mRNAs in macrophages in vitro. We confirmed this sequential decay model in vivo since LPS-treated mice with myeloid TTP ablation exhibited similar cytokine dysregulation profile as macrophages. The mice were hypersensitive to LPS but otherwise healthy with no signs of hyperinflammation seen in conventional TTP knockout mice demonstrating the requirement for myeloid TTP in re-installment but not maintenance of immune homeostasis. These findings reveal a TTP- and p38 MAPK-dominated regulatory mechanism that is vital for balancing acute inflammation by a temporally and qualitatively controlled mRNA decay.
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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.