ArticleMolecular and cellular biology2000
Somatic mRNA turnover mutants implicate tristetraprolin in the interleukin-3 mRNA degradation pathway.
Article in Molecular and cellular biology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.
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Who cites it
73 citing papers in PubMed, 152 citations in OpenAlex.
- Multivalent interactions with CCR4-NOT and PABPC1 determine mRNA repression efficiency by tristetraprolin.Nature communications · 2025Article
- The multifaceted role of Fragile X-Related Protein 1 (FXR1) in cellular processes: an updated review on cancer and clinical applications.Cell death & disease · 2024Review
- Shaping the Innate Immune Response Through Post-Transcriptional Regulation of Gene Expression Mediated by RNA-Binding Proteins.Frontiers in immunology · 2021Review
- Review
- Bone marrow deficiency of mRNA decaying protein Tristetraprolin increases inflammation and mitochondrial ROS but reduces hepatic lipoprotein production in LDLR knockout mice.Redox biology · 2020Article
- Tristetraprolin specifically regulates the expression and alternative splicing of immune response genes in HeLa cells.BMC immunology · 2019Article
- RNA Degradation in Neurodegenerative Disease.Advances in neurobiology · 2018Review
- A balancing act: RNA binding protein HuR/TTP axis in endometriosis patients.Scientific reports · 2017Article
- Pterostilbene 4'-Oxidative medicine and cellular longevity · 2017Article
- Can we observe changes in mRNA "state"? Overview of methods to study mRNA interactions with regulatory proteins relevant in cancer related processes.The Analyst · 2016Review
- Post-transcriptional Regulation of Immunological Responses through Riboclustering.Frontiers in immunology · 2016Review
- The GroEL protein of Porphyromonas gingivalis regulates atherogenic phenomena in endothelial cells mediated by upregulating toll-like receptor 4 expression.American journal of translational research · 2016Article
- Post-transcriptional regulation of DNA damage-responsive gene expression.Antioxidants & redox signaling · 2014Review
- Post-transcriptional regulatory networks in immunity.Immunological reviews · 2013Review
- Article
- The role of tristetraprolin in cancer and inflammation.Frontiers in bioscience (Landmark edition) · 2012Review
- ZFP36L1 negatively regulates plasmacytoid differentiation of BCL1 cells by targeting BLIMP1 mRNA.PloS one · 2012Article
- Article
- Downregulation of the AU-rich RNA-binding protein ZFP36 in chronic HBV patients: implications for anti-inflammatory therapy.PloS one · 2012Article
- A molecular mechanism for TNF-α-mediated downregulation of B cell responses.Journal of immunology (Baltimore, Md. : 1950) · 2012Article
13 more citing papers are in PubMed but not listed here.
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PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Control of mRNA stability is critical for expression of short-lived transcripts from cytokines and proto-oncogenes. Regulation involves an AU-rich element (ARE) in the 3' untranslated region (3'UTR) and cognate trans-acting factors thought to promote either degradation or stabilization of the mRNA. In this study we present a novel approach using somatic cell genetics designed to identify regulators of interleukin-3 (IL-3) mRNA turnover. Mutant cell lines were generated from diploid HT1080 cells transfected with a reporter construct containing green fluorescent protein (GFP) linked to the IL-3 3'UTR. GFP was expressed at low levels due to rapid decay of the mRNA. Following chemical mutagenesis and selection of GFP-overexpressing cells, we could isolate three mutant clones (slowA, slowB, and slowC) with a specific, trans-acting defect in IL-3 mRNA degradation, while the stability of IL-2 and tumor necrosis factor alpha reporter transcripts was not affected. Somatic cell fusion experiments revealed that the mutants are genetically recessive and form two complementation groups. Expression of the tristetraprolin gene in both groups led to reversion of the mutant phenotype, thereby linking this gene to the IL-3 mRNA degradation pathway. The genetic approach described here should allow identification of the defective functions by gene transfer and is also applicable to the study of other mRNA turnover pathways.
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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.