ArticleJournal of immunology (Baltimore, Md. : 1950)2008
Role of the RNA-binding protein tristetraprolin in glucocorticoid-mediated gene regulation.
Article in Journal of immunology (Baltimore, Md. : 1950), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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Who cites it
53 citing papers in PubMed, 95 citations in OpenAlex.
- The ZFP36 Family as Post-Transcriptional Regulators in Physiology and Disease.International journal of molecular sciences · 2026Review
- Restraint of inflammasome-driven cytokine responses through the mRNA stability protein TTP.Cell reports · 2025Article
- Bridging the Nervous-Endocrine System and Immune Response, in Human Chagas Disease Pathology.Neuroimmunomodulation · 2025Review
- Role of glucocorticoid receptor expression in Chronic Chagas Cardiomyopathy: implications for inflammation and cardiac hypertrophy.Frontiers in endocrinology · 2025Article
- Global analysis of the abundance of AU-rich mRNAs in response to glucocorticoid treatment.Scientific reports · 2024Article
- Overview on the Link Between the Complement System and Auto-Immune Articular and Pulmonary Disease.Open access rheumatology : research and reviews · 2023Review
- The RNA binding proteinsFrontiers in cell and developmental biology · 2023Article
- FOXO1 Is a Key Mediator of Glucocorticoid-Induced Expression of Tristetraprolin in MDA-MB-231 Breast Cancer Cells.International journal of molecular sciences · 2022Article
- Differential Effects of Toll-Like Receptor Activation and Differential Mediation by MAP Kinases of Immune Responses in Microglial Cells.Cellular and molecular neurobiology · 2022Article
- miR‑146a‑5p negatively regulates the IL‑1β‑stimulated inflammatory response via downregulation of the IRAK1/TRAF6 signaling pathway in human intestinal epithelial cells.Experimental and therapeutic medicine · 2022Article
- Integrative analysis of macrophage ribo-Seq and RNA-Seq data define glucocorticoid receptor regulated inflammatory response genes into distinct regulatory classes.Computational and structural biotechnology journal · 2022Article
- Tristetraprolin limits age-related expansion of myeloid-derived suppressor cells.Frontiers in immunology · 2022Article
- Aberrant Post-Transcriptional Regulation of Protein Expression in the Development of Chronic Obstructive Pulmonary Disease.International journal of molecular sciences · 2021Review
- Decoding the temporal nature of brain GR activity in the NFκB signal transition leading to depressive-like behavior.Molecular psychiatry · 2021Article
- Review
- The gut microbiota metabolite urolithin A inhibits NF-κB activation in LPS stimulated BMDMs.Scientific reports · 2021Article
- Identification of an AP1-ZFP36 Regulatory Network Associated with Breast Cancer Prognosis.Journal of mammary gland biology and neoplasia · 2020Article
- Posttranscriptional Gene Regulatory Networks in Chronic Airway Inflammatory Diseases:Frontiers in immunology · 2020Article
- Fighting the Fire: Mechanisms of Inflammatory Gene Regulation by the Glucocorticoid Receptor.Frontiers in immunology · 2019Review
- Expression of the mRNA stability regulator Tristetraprolin is required for lactation maintenance in the mouse mammary gland.Oncotarget · 2018Article
Corrections and comments
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Authors and funding
8 authors at 5 institutions in 1 country.
Funding
Abstract
Glucocorticoids (GCs) are the mainstay of anti-inflammatory therapy. Modulation of posttranscriptional regulation (PTR) of gene expression by GCs is a relevant yet poorly characterized mechanism of their action. The RNA-binding protein tristetraprolin (TTP) plays a central role in PTR by binding to AU-rich elements in the 3'-untranslated region of proinflammatory transcripts and accelerating their decay. We found that GCs induce TTP expression in primary and immortalized human bronchial epithelial cells. To investigate the importance of PTR and the role of TTP in GC function, we compared the effect of GC treatment on genome-wide gene expression using mouse embryonic fibroblasts (MEFs) obtained from wild-type and TTP(-/-) mice. We confirmed that GCs induce TTP in MEFs and observed in TTP(-/-) MEFs a striking loss of up to 85% of GC-mediated gene expression. Gene regulation by TNF-alpha was similarly affected, as was the antagonistic effect of GC on TNF-alpha-induced response. Inflammatory genes, including cytokines and chemokines, were among the genes whose sensitivity to GCs was affected by lack of TTP. Silencing of TTP in WT MEFs by small interfering RNA confirmed loss of GC response in selected targets. Immunoprecipitation of ribonucleoprotein complexes revealed binding of TTP to several validated transcripts. Changes in the rate of transcript degradation studied by actinomycin D were documented for only a subset of transcripts bound to TTP. These results reveal a strong and previously unrecognized contribution of PTR to the anti-inflammatory action of GCs and point at TTP as a key factor mediating this process through a complex mechanism of action.
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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.