ArticleMolecular and cellular biology2011
Phosphorylation of tristetraprolin by MK2 impairs AU-rich element mRNA decay by preventing deadenylase recruitment.
Article in Molecular and cellular biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 118 papers.
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Who cites it
118 citing papers in PubMed, 189 citations in OpenAlex.
- Phase II randomised, placebo-controlled study to evaluate the efficacy and safety of an MK2 inhibitor in ankylosing spondylitis.RMD open · 2026Trial
- CC-99677, a novel, oral, selective covalent MK2 inhibitor, sustainably reduces pro-inflammatory cytokine production.Arthritis research & therapy · 2022Trial
- The lysosomal LAMTOR-Rag complex functions as a checkpoint for antiviral interferon production.The EMBO journal · 2026Article
- Multivalent interactions with CCR4-NOT and PABPC1 determine mRNA repression efficiency by tristetraprolin.Nature communications · 2025Article
- Exploring the CNOT1(800-999) HEAT Domain and Its Interactions with Tristetraprolin (TTP) as Revealed by Hydrogen/Deuterium Exchange Mass Spectrometry.Biomolecules · 2025Article
- Shiga Toxins Produced by EnterohaemorrhagicJournal of microbiology and biotechnology · 2024Article
- Loss of MK2 Enhances Radiation-Mediated Apoptosis in Bladder Cancer.World journal of oncology · 2024Article
- Regulation of Zfp36 by ISGF3 and MK2 restricts the expression of inflammatory cytokines during necroptosis stimulation.Cell death & disease · 2024Article
- Tankyrase-1 regulates RBP-mediated mRNA turnover to promote muscle fiber formation.Nucleic acids research · 2024Article
- Post-transcriptional regulation of BIRC5/survivin expression and induction of apoptosis in breast cancer cells by tristetraprolin.RNA biology · 2024Article
- NPPC and AREG supplementation in IVM systems alter mRNA translation and decay programs-related gene expression in bovine COC.Animal reproduction · 2024Article
- Identification of Glucocorticoid Receptor Target Genes That Potentially Inhibit Collagen Synthesis in Human Dermal Fibroblasts.Biomolecules · 2023Article
- The nexus between RNA-binding proteins and their effectors.Nature reviews. Genetics · 2023Review
- Role of ubiquitin regulatory X domain‑containing protein 3B in the development of hepatocellular carcinoma (Review).Oncology reports · 2023Review
- Retinoid metabolism: new insights.Journal of molecular endocrinology · 2022Review
- The ZFP36 family of RNA binding proteins regulates homeostatic and autoreactive T cell responses.Science immunology · 2022Article
- The Conserved CNOT1 Interaction Motif of Tristetraprolin Regulates ARE-mRNA Decay Independently of the p38 MAPK-MK2 Kinase Pathway.Molecular and cellular biology · 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
- Mitogen-activated protein kinase-activated protein kinase-2 (MK2) and its role in cell survival, inflammatory signaling, and migration in promoting cancer.Molecular carcinogenesis · 2022Article
- Review
58 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors at 4 institutions in 3 countries.
Funding
Abstract
mRNA turnover is a critical step in the control of gene expression. In mammalian cells, a subset of mRNAs regulated at the level of mRNA turnover contain destabilizing AU-rich elements (AREs) in their 3' untranslated regions. These transcripts are bound by a suite of ARE-binding proteins (AUBPs) that receive information from cell signaling events to modulate rates of ARE mRNA decay. Here we show that a key destabilizing AUBP, tristetraprolin (TTP), is repressed by the p38 mitogen-activated protein kinase (MAPK)-activated kinase MK2 due to the inability of phospho-TTP to recruit deadenylases to target mRNAs. TTP is tightly associated with cytoplasmic deadenylases and promotes rapid deadenylation of target mRNAs both in vitro and in cells. TTP can direct the deadenylation of substrate mRNAs when tethered to a heterologous mRNA, yet its ability to do so is inhibited upon phosphorylation by MK2. Phospho-TTP is not impaired in mRNA binding but does fail to recruit the major cytoplasmic deadenylases. These observations suggest that phosphorylation of TTP by MK2 primarily affects mRNA decay downstream of RNA binding by preventing recruitment of the deadenylation machinery. Thus, TTP may remain poised to rapidly reactivate deadenylation of bound transcripts to downregulate gene expression once the p38 MAPK pathway is deactivated.
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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.