ReviewBiochemical Society transactions2016
The control of inflammation via the phosphorylation and dephosphorylation of tristetraprolin: a tale of two phosphatases.
Review in Biochemical Society transactions, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
56 citing papers in PubMed, 81 citations in OpenAlex.
- ZFP36 Family Proteins as Critical Regulators of Inflammation, Immune Cell Development, and Antiviral Responses.Vaccines · 2026Review
- The ZFP36 Family as Post-Transcriptional Regulators in Physiology and Disease.International journal of molecular sciences · 2026Review
- The ZFP36 Family as a Post-Transcriptional Immune Checkpoint in Immunity and Disease: Molecular Mechanisms and Functional Implications.Biomolecules · 2026Review
- Tristetraprolin attenuates schistosomiasis-induced liver fibrosis through m⁶A-mediated regulation of TGF-β1 mRNA stability.PLoS pathogens · 2026Article
- Dissecting temporal regulation of the TLR4-IL-6 axis using systematic targeted inhibition.Scientific reports · 2026Article
- Functional interplay between TTP/ZFP36 and HuR/ELAVL1 in cancer: a post-transcriptional regulatory network.Frontiers in oncology · 2026Review
- Beyond cartilage degeneration: osteoarthritis as a systems failure of inflammation regulation.Frontiers in medicine · 2026Article
- Differential Regulation of TCR-Induced ZFP36 and ZFP36L1 Expression by Cyclosporin A in CD8European journal of immunology · 2025Article
- Multivalent interactions with CCR4-NOT and PABPC1 determine mRNA repression efficiency by tristetraprolin.Nature communications · 2025Article
- Dietary Fermentation withInternational journal of molecular sciences · 2025Article
- Review
- Restraint of inflammasome-driven cytokine responses through the mRNA stability protein TTP.Cell reports · 2025Article
- Review
- Integrative bioinformatics analysis reveals novel insights into osteoarthritis pathogenesis and diagnostic biomarkers.BMC musculoskeletal disorders · 2024Article
- Combined transcriptome and metabolome analysis reveals breed-specific regulatory mechanisms in Dorper and Tan sheep.BMC genomics · 2024Article
- Bioinformatics-led discovery of ferroptosis-associated diagnostic biomarkers and molecule subtypes for tuberculosis patients.European journal of medical research · 2023Article
- Non-coding RNAs and Exosomal Non-coding RNAs in Traumatic Brain Injury: the Small Player with Big Actions.Molecular neurobiology · 2023Review
- HUWE1 controls tristetraprolin proteasomal degradation by regulating its phosphorylation.eLife · 2023Article
- Clinical implications of tristetraprolin (TTP) modulation in the treatment of inflammatory diseases.Pharmacology & therapeutics · 2022Review
- The Conserved CNOT1 Interaction Motif of Tristetraprolin Regulates ARE-mRNA Decay Independently of the p38 MAPK-MK2 Kinase Pathway.Molecular and cellular biology · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Twenty years ago, the first description of a tristetraprolin (TTP) knockout mouse highlighted the fundamental role of TTP in the restraint of inflammation. Since then, work from several groups has generated a detailed picture of the expression and function of TTP. It is a sequence-specific RNA-binding protein that orchestrates the deadenylation and degradation of several mRNAs encoding inflammatory mediators. It is very extensively post-translationally modified, with more than 30 phosphorylations that are supported by at least two independent lines of evidence. The phosphorylation of two particular residues, serines 52 and 178 of mouse TTP (serines 60 and 186 of the human orthologue), has profound effects on the expression, function and localisation of TTP. Here, we discuss the control of TTP biology via its phosphorylation and dephosphorylation, with a particular focus on recent advances and on questions that remain unanswered.
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What OpenQuestion holds
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.