ArticleJournal of inflammation (London, England)2015
Functional regulation of Zfp36l1 and Zfp36l2 in response to lipopolysaccharide in mouse RAW264.7 macrophages.
Article in Journal of inflammation (London, England), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 36 citations in OpenAlex.
- The ZFP36 Family as a Post-Transcriptional Immune Checkpoint in Immunity and Disease: Molecular Mechanisms and Functional Implications.Biomolecules · 2026Review
- Dual-Network Protein Hydrogels Promote Rapid Hemostasis and Immune-Regulated Scarless Tissue Regeneration.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Glucocorticoid-Induced Proteome and Phosphoproteome Changes in Breast Cancer Cell Lines.Journal of proteome research · 2026Article
- Decoding cross-talk between Mpox and HIV: insights from transcriptomics and network-based analyses.Virology journal · 2025Article
- Single nuclei RNA-sequencing unveils alveolar macrophages as drivers of endothelial damage in obese HFpEF-related pulmonary hypertension.Cardiovascular diabetology · 2025Article
- Review
- Lipopolysaccharide regulation of antiinflammatory tristetraprolin family and proinflammatory gene expression in mouse macrophages.BMC research notes · 2024Article
- NPPC and AREG supplementation in IVM systems alter mRNA translation and decay programs-related gene expression in bovine COC.Animal reproduction · 2024Article
- ZFP36 ring finger protein like 1 significantly suppresses human coronavirus OC43 replication.PeerJ · 2023Article
- Dynamic and widespread control of poly(A) tail length during macrophage activation.RNA (New York, N.Y.) · 2022Article
- Sequence and tissue targeting specificity of ZFP36L2 reveals Elavl2 as a novel target with co-regulation potential.Nucleic acids research · 2022Article
- Zinc Finger Protein ZFP36L1 Inhibits Flavivirus Infection by both 5'-3' XRN1 and 3'-5' RNA-Exosome RNA Decay Pathways.Journal of virology · 2022Article
- Targeted Re-Sequencing of the 2p21 Locus Identifies Non-Syndromic Cleft Lip Only Novel Susceptibility GeneFrontiers in genetics · 2022Article
- Identification of diagnostic signatures associated with immune infiltration in Alzheimer's disease by integrating bioinformatic analysis and machine-learning strategies.Frontiers in aging neuroscience · 2022Article
- The functional characterization of phosphorylation of tristetraprolin at C-terminal NOT1-binding domain.Journal of inflammation (London, England) · 2021Article
- RNA-Binding Protein ZFP36L2 Downregulates Helios Expression and Suppresses the Function of Regulatory T Cells.Frontiers in immunology · 2020Article
- Genetic Analyses of Tanzanian Local Chicken Ecotypes Challenged with Newcastle Disease Virus.Genes · 2019Article
- Control of cytokine mRNA degradation by the histone deacetylase inhibitor ITF2357 in rheumatoid arthritis fibroblast-like synoviocytes: beyond transcriptional regulation.Arthritis research & therapy · 2018Article
- Alternative splicing analysis in human monocytes and macrophages reveals MBNL1 as major regulator.Nucleic acids research · 2018Article
- RNA-binding proteins control gene expression and cell fate in the immune system.Nature immunology · 2018Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe tristetraprolin (TTP) family of mRNA-binding proteins contains three major members, Ttp, Zfp36l1, and Zfp36l2. Ttp down-regulates the stability of AU-rich element-containing mRNAs and functions as an anti-inflammation regulator.
methodsTo examine whether other TTP family proteins also play roles in the inflammatory response, their expression profiles and the possible mRNA targets were determined in the knockdown cells.
resultsTtp mRNA and protein were highly induced by lipopolysaccharide (LPS), whereas Zfp36l1 and Zfp36l2 mRNAs were down-regulated and their proteins were phosphorylated during early lipopolysaccharide stimulation. Biochemical and functional analyses exhibited that the decrease of Zfp36l2 mRNA was cross-regulated by Ttp. Knockdown of Zfp36l1 and Zfp36l2 increased the basal level of Mkp-1 mRNAs by prolonging its half-life. Increasing the expression of Mkp-1 inhibited the activation of p38 MAPK under lipopolysaccharide stimulation and down-regulated Tnfα, and Ttp mRNA. In addition, hyper-phosphorylation of Zfp36l1 might stabilize Mkp-1 expression by forming a complex with the adapter protein 14-3-3 and decreasing the interaction with deadenylase Caf1a.
conclusionsOur findings imply that the expression and phosphorylation of Zfp36l1 and Zfp36l2 may modulate the basal level of Mkp-1 mRNA to control p38 MAPK activity during lipopolysaccharide stimulation, which would affect the inflammatory mediators production. Zfp36l1 and Zfp36l2 are important regulators of the innate immune response.
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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.