ArticleRNA biology2019
Bi-phased regulation of the post-transcriptional inflammatory response by Tristetraprolin levels.
Article in RNA biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 21 citations in OpenAlex.
- Profound alterations of cancer transcriptomes by the RNase L inhibitor ABCE1 through the modulation of UU/UA-dinucleotide rich transcript abundance.RNA biology · 2026Article
- RNA-binding protein tristetraprolin inhibits Th2 cell activation and differentiation in allergic rhinitis by promoting TRIM18 mRNA decay.The Journal of biological chemistry · 2026Article
- Restraint of inflammasome-driven cytokine responses through the mRNA stability protein TTP.Cell reports · 2025Article
- A Computational Recognition Analysis of Promising Prognostic Biomarkers in Breast, Colon and Lung Cancer Patients.International journal of molecular sciences · 2025Article
- The short conserved region-2 of LARP4 interacts with ribosome-associated RACK1 and promotes translation.Nucleic acids research · 2025Article
- The short conserved region-2 of LARP4 interacts with ribosome-associated RACK1 and promotes translation.bioRxiv : the preprint server for biology · 2024Article
- Global analysis of the abundance of AU-rich mRNAs in response to glucocorticoid treatment.Scientific reports · 2024Article
- Differential upregulation of AU-rich element-containing mRNAs in COVID-19.Human genomics · 2022Article
- Post-transcriptional screen of cancer amplified genes identifies ERBB2/Her2 signaling as AU-rich mRNA stability-promoting pathway.Oncogenesis · 2021Article
- Kinome inhibition reveals a role for polo-like kinase 1 in targeting post-transcriptional control in cancer.Molecular oncology · 2021Article
- ZFP36 protects lungs from intestinal I/R-induced injury and fibrosis through the CREBBP/p53/p21/Bax pathway.Cell death & disease · 2021Article
- Review
- Conceptual Advances in Control of Inflammation by the RNA-Binding Protein Tristetraprolin.Frontiers in immunology · 2021Review
- Wnt/CTNNB1 Signal Transduction Pathway Inhibits the Expression of ZFP36 in Squamous Cell Carcinoma, by Inducing Transcriptional Repressors SNAI1, SLUG and TWIST.International journal of molecular sciences · 2020Article
- Identification of biomarkers in common chronic lung diseases by co-expression networks and drug-target interactions analysis.Molecular medicine (Cambridge, Mass.) · 2020Article
- Tristetraprolin Overexpression in Non-hematopoietic Cells Protects Against Acute Lung Injury in Mice.Frontiers in immunology · 2020Article
- Post-Transcriptional Inflammatory Response to Intracellular Bacterial c-di-AMP.Frontiers in immunology · 2019Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
AU-rich elements (AREs) are cis-acting instability and translation inhibition elements that are present in the 3'UTR of most inducible inflammatory mRNAs such as TNF and Cxcl2. mRNAs that contain AREs are, by default, repressed and only transiently expressed in response to stimuli. They are targeted by the inducible RNA-binding protein Tristetraprolin (TTP) which blocks their translation and facilitates their decay, thereby contributing to the quick termination of their expression. The exogenous over-expression of TTP in HEK293 cells can unexpectedly lead to the upregulation and extended expression of a nanoLuciferase reporter that contains the ARE of TNF. Here we show that, a moderate downregulation of the highly expressed endogenous TTP after LPS induction by siRNA in macrophages can lead to a reduction in the release of TNF and Cxcl2. We propose that, in contrast to their canonical function, very high levels of induced TTP at the onset of the inflammatory response can enhance the expression of ARE-mRNAs at the post-transcriptional level, independently of phosphorylation status. As the inflammatory response progresses, TTP levels diminish but they continuously regain their ability to reduce the expression of ARE-mRNAs to reach a turning point of 'optimal TTP level' with a maximum ability to repress ARE-mRNA expression. Below this level, a further reduction in TTP levels now leads to the loss of canonical-TTP function resulting in increased ARE-mRNA expression. These novel findings should contribute to the understanding of feedback loops that control the kinetics of the inflammatory response.
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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.