ArticleProceedings of the National Academy of Sciences of the United States of America2002
Ubiquitin-dependent mechanism regulates rapid turnover of AU-rich cytokine mRNAs.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 101 citations in OpenAlex.
- ZFP36 Family Proteins as Critical Regulators of Inflammation, Immune Cell Development, and Antiviral Responses.Vaccines · 2026Review
- Expression of targets of the RNA-binding protein AUF-1 in human airway epithelium indicates its role in cellular senescence and inflammation.Frontiers in immunology · 2023Article
- The Emerging Role of STING in Insect Innate Immune Responses and Pathogen Evasion Strategies.Frontiers in immunology · 2022Review
- Article
- Changes to the identity of EndoC-βH1 beta cells may be mediated by stress-induced depletion of HNRNPD.Cell & bioscience · 2021Article
- MKRN2 is a novel ubiquitin E3 ligase for the p65 subunit of NF-κB and negatively regulates inflammatory responses.Scientific reports · 2017Article
- Lipopolysaccharide (LPS)-stimulated iNOS Induction Is Increased by Glucosamine under Normal Glucose Conditions but Is Inhibited by Glucosamine under High Glucose Conditions in Macrophage Cells.The Journal of biological chemistry · 2017Article
- Article
- Roles of myeloperoxidase and GAPDH in interferon-gamma production of GM-CSF-dependent macrophages.Heliyon · 2016Article
- A non-proteolytic role for ubiquitin in deadenylation of MHC-I mRNA by the RNA-binding E3-ligase MEX-3C.Nature communications · 2015Article
- Regulation of AU-Rich Element RNA Binding Proteins by Phosphorylation and the Prolyl Isomerase Pin1.Biomolecules · 2015Review
- Signaling pathways that control mRNA turnover.Cellular signalling · 2013Review
- Article
- The prolyl isomerase Pin1 targets stem-loop binding protein (SLBP) to dissociate the SLBP-histone mRNA complex linking histone mRNA decay with SLBP ubiquitination.Molecular and cellular biology · 2012Article
- AU-rich element-binding protein negatively regulates CCAAT enhancer-binding protein mRNA stability during long-term synaptic plasticity in Aplysia.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- The RNA-binding E3 ubiquitin ligase MEX-3C links ubiquitination with MHC-I mRNA degradation.The EMBO journal · 2012Article
- Association of the von Hippel-Lindau protein with AUF1 and posttranscriptional regulation of VEGFA mRNA.Molecular cancer research : MCR · 2012Article
- Modulation of neoplastic gene regulatory pathways by the RNA-binding factor AUF1.Frontiers in bioscience (Landmark edition) · 2011Review
- Links between innate immunity and normal tissue radiobiology.Radiation research · 2010Review
- Phosphorylation of human tristetraprolin in response to its interaction with the Cbl interacting protein CIN85.PloS one · 2010Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
An AU rich element (ARE) in the 3' noncoding region promotes the rapid degradation of mammalian cytokine and proto-oncogene mRNAs, such as tumor necrosis factor-alpha, granulocyte-macrophage colony-stimulating factor (GM-CSF) and c-fos. Destabilization of ARE-mRNAs involves the association of ARE-binding proteins tristetraprolin or AUF1 and proteasome activity, of which the latter has not been characterized. Here, we show that the stability of a model short-lived mRNA containing the GM-CSF ARE was regulated by the level of ubiquitin-conjugating activity in the cell, which links ARE-mRNA decay to proteasome activity. Increased expression of a cytokine-inducible deubiquitinating protein (DUB) that impairs addition of ubiquitin to proteins fully blocked ARE-mRNA decay, whereas increased expression of a DUB that promotes ubiquitin addition to proteins strongly accelerated ARE-mRNA decay. ARE-mRNA turnover was found to be activated by the ubiquitin-addition reaction and blocked by the ubiquitin-removal reaction. Saturation of the ARE-mRNA decay machinery by high levels of ARE-mRNA, which is well established but not understood, was found to be relieved by increased expression of a DUB that promotes ubiquitin addition to proteins. Finally, inhibition of proteasome activity also blocked accelerated ARE-mRNA decay that is mediated by increased ubiquitin recycling. These results demonstrate that both ubiquitinating activity and proteasome activity are essential for rapid turnover of a model cytokine ARE-mRNA containing the GM-CSF ARE.
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