ArticleMolecular and cellular biology2003
A constitutive decay element promotes tumor necrosis factor alpha mRNA degradation via an AU-rich element-independent pathway.
Article in Molecular and cellular biology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
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Who cites it
56 citing papers in PubMed.
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- Regulation and Function of the Atypical IκBs-Bcl-3, IκBEuropean journal of immunology · 2025Review
- The role of structure in regulatory RNA elements.Bioscience reports · 2024Review
- Crosstalk between Regnase-1 and -3 shapes mast cell survival and cytokine expression.Life science alliance · 2024Article
- Suppression of Pro-Inflammatory M1 Polarization of LPS-Stimulated RAW 264.7 Macrophage Cells by Fucoxanthin-RichMarine drugs · 2023Article
- TRAIL promotes the polarization of human macrophages toward a proinflammatory M1 phenotype and is associated with increased survival in cancer patients with high tumor macrophage content.Frontiers in immunology · 2023Article
- NMR-derived secondary structure of the full-length Ox40 mRNA 3'UTR and its multivalent binding to the immunoregulatory RBP Roquin.Nucleic acids research · 2022Article
- ZC3H12C expression in dendritic cells is necessary to prevent lymphadenopathy of skin-draining lymph nodes.Immunology and cell biology · 2022Article
- Tumor necrosis factor is a necroptosis-associated alarmin.Frontiers in immunology · 2022Article
- The relationship of mRNA with protein expression in CD8+ T cells associates with gene class and gene characteristics.PloS one · 2022Article
- Sequence determinants as key regulators in gene expression of T cells.Immunological reviews · 2021Review
- Post-transcriptional control of T-cell cytokine production: Implications for cancer therapy.Immunology · 2021Review
- Shaping the Innate Immune Response Through Post-Transcriptional Regulation of Gene Expression Mediated by RNA-Binding Proteins.Frontiers in immunology · 2021Review
- Appetite Regulation of TLR4-Induced Inflammatory Signaling.Frontiers in endocrinology · 2021Review
- Structural basis for the recognition of transiently structured AU-rich elements by Roquin.Nucleic acids research · 2020Article
- Human T cells employ conserved AU-rich elements to fine-tune IFN-γ production.European journal of immunology · 2020Article
- Post-transcriptional regulation of inflammation by RNA-binding proteins via cis-elements of mRNAs.Journal of biochemistry · 2019Review
- UPFront and center in RNA decay: UPF1 in nonsense-mediated mRNA decay and beyond.RNA (New York, N.Y.) · 2019Review
- A translational silencing function of MCPIP1/Regnase-1 specified by the target site context.Nucleic acids research · 2018Article
- Short-lived AUF1 p42-binding mRNAs of RANKL and BCL6 have two distinct instability elements each.PloS one · 2018Article
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tumor necrosis factor alpha (TNF-alpha) expression is regulated by transcriptional as well as posttranscriptional mechanisms, the latter including the control of mRNA decay through an AU-rich element (ARE) in the 3' untranslated region (UTR). Using two mutant cell lines deficient for ARE-mediated mRNA decay, we provide evidence for a second element, the constitutive decay element (CDE), which is also located in the 3' UTR of TNF-alpha. In stably transfected RAW 264.7 macrophages stimulated with lipopolysaccharide (LPS), the CDE continues to target a reporter transcript for rapid decay, whereas ARE-mediated decay is blocked. Similarly, the activation of p38 kinase and phosphatidylinositol 3-kinase in NIH 3T3 cells inhibits ARE-mediated but not CDE-mediated mRNA decay. The CDE was mapped to an 80-nucleotide (nt) segment downstream of the ARE, and point mutation analysis identified within the CDE a conserved sequence of 15 nt that is required for decay activity. We propose that the CDE represses TNF-alpha expression by maintaining the mRNA short-lived, thereby preventing excessive induction of TNF-alpha after LPS stimulation. Thus, CDE-mediated mRNA decay is likely to be an important mechanism limiting LPS-induced pathologic processes.
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