ArticleJournal of leukocyte biology2015
Tristetraprolin (TTP) coordinately regulates primary and secondary cellular responses to proinflammatory stimuli.
Article in Journal of leukocyte biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 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
37 citing papers in PubMed, 44 citations in OpenAlex.
- ZFP36 Family Proteins as Critical Regulators of Inflammation, Immune Cell Development, and Antiviral Responses.Vaccines · 2026Review
- Endothelin-1 induces Zfp36 family RNA-binding proteins and restrains cytokine and chemokine production in reactive astrocytes.The Journal of biological chemistry · 2026Article
- Synergistic roles of tristetraprolin family members in myeloid cells in the control of inflammation.Life science alliance · 2024Article
- ZFP36-mediated mRNA decay regulates metabolism.Cell reports · 2023Article
- Genome-wide analysis of RNA-binding proteins co-expression with alternative splicing events in mitral valve prolapse.Frontiers in immunology · 2023Article
- Clinical implications of tristetraprolin (TTP) modulation in the treatment of inflammatory diseases.Pharmacology & therapeutics · 2022Review
- STAT3 regulates inflammatory cytokine production downstream of TNFR1 by inducing expression of TNFAIP3/A20.Journal of cellular and molecular medicine · 2022Article
- Snapshots of nascent RNA reveal cell- and stimulus-specific responses to acute kidney injury.JCI insight · 2022Article
- Activation of the MKK3-p38-MK2-ZFP36 Axis by Coronavirus Infection Restricts the Upregulation of AU-Rich Element-Containing Transcripts in Proinflammatory Responses.Journal of virology · 2022Article
- Review
- Tristetraprolin, Inflammation, and Metabolic Syndrome in Arab Adults: A Case Control Study.Biology · 2021Article
- Article
- Regional differences in use of immune-modulating catechins should be investigated regarding COVID-19.Brain, behavior, and immunity · 2020Article
- The Tristetraprolin Family of RNA-Binding Proteins in Cancer: Progress and Future Prospects.Cancers · 2020Review
- Tristetraprolin Regulates TFrontiers in immunology · 2020Article
- Regulated Tristetraprolin Overexpression Dampens the Development and Pathogenesis of Experimental Autoimmune Uveitis.Frontiers in immunology · 2020Article
- Tristetraprolin Overexpression in Non-hematopoietic Cells Protects Against Acute Lung Injury in Mice.Frontiers in immunology · 2020Article
- High accuracy gene expression profiling of sorted cell subpopulations from breast cancer PDX model tissue.PloS one · 2020Article
- Importance of the Conserved Carboxyl-Terminal CNOT1 Binding Domain to Tristetraprolin ActivityMolecular and cellular biology · 2019Article
- Thymoquinone-Induced Tristetraprolin Inhibits Tumor Growth and Metastasis through Destabilization of MUC4 mRNA.International journal of molecular sciences · 2019Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
TTP is an anti-inflammatory protein that acts by binding to AREs in its target mRNAs, such as Tnf mRNA, and promoting their deadenylation and decay. TNF released from inflammatory cells can then stimulate gene expression in tissue cells, such as fibroblasts. To determine whether TTP could affect the decay of TNF-induced transcripts in fibroblasts, we exposed primary embryonic fibroblasts and stable fibroblast cell lines, derived from WT and TTP KO mice, to TNF. The decay rates of transcripts encoded by several early-response genes, including Cxcl1, Cxcl2, Ier3, Ptgs2, and Lif, were significantly slowed in TTP-deficient fibroblasts after TNF stimulation. These changes were associated with TTP-dependent increases in CXCL1, CXCL2, and IER3 protein levels. The TTP-susceptible transcripts contained multiple, conserved, closely spaced, potential TTP binding sites in their 3'-UTRs. WT TTP, but not a nonbinding TTP zinc finger mutant, bound to RNA probes that were based on the mRNA sequences of Cxcl1, Cxcl2, Ptgs2, and Lif. TTP-promoted decay of transcripts encoding chemokines and other proinflammatory mediators is thus a critical post-transcriptional regulatory mechanism in the response of secondary cells, such as fibroblasts, to TNF released from primary immune cells.
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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.