ArticleNucleic acids research2018
A translational silencing function of MCPIP1/Regnase-1 specified by the target site context.
Article in Nucleic acids research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 29 citations in OpenAlex.
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- The RNA binding protein Arid5a drives IL-17-dependent autoantibody-induced glomerulonephritis.The Journal of experimental medicine · 2024Article
- The Nuclear NF-κB Regulator IκBζ: Updates on Its Molecular Functions and Pathophysiological Roles.Cells · 2024Review
- Crosstalk between Regnase-1 and -3 shapes mast cell survival and cytokine expression.Life science alliance · 2024Article
- Oncogene-induced MALT1 protease activity drives posttranscriptional gene expression in malignant lymphomas.Blood · 2023Article
- IL-17A and TNF synergistically drive expression of proinflammatory mediators in synovial fibroblasts via IκBζ-dependent induction of ELF3.Rheumatology (Oxford, England) · 2023Article
- Cooperation of RNA-Binding Proteins - a Focus on Roquin Function in T Cells.Frontiers in immunology · 2022Review
- Sequence determinants as key regulators in gene expression of T cells.Immunological reviews · 2021Review
- Terminal uridyltransferase 7 regulates TLR4-triggered inflammation by controlling Regnase-1 mRNA uridylation and degradation.Nature communications · 2021Article
- Regnase-1 is essential for B cell homeostasis to prevent immunopathology.The Journal of experimental medicine · 2021Article
- MCPIP1 ribonuclease can bind and cleaveRNA biology · 2021Article
- Macrophage Regnase-1 Deletion Deteriorates Liver Ischemia/Reperfusion Injury Through Regulation of Macrophage Polarization.Frontiers in physiology · 2020Article
- Immediate and deferred epigenomic signatures of in vivo neuronal activation in mouse hippocampus.Nature neuroscience · 2019Article
- Translation-dependent unwinding of stem-loops by UPF1 licenses Regnase-1 to degrade inflammatory mRNAs.Nucleic acids research · 2019Article
- Regnase-1-mediated post-transcriptional regulation is essential for hematopoietic stem and progenitor cell homeostasis.Nature communications · 2019Article
- Ethyl pyruvate reduces organic dust-induced airway inflammation by targeting HMGB1-RAGE signaling.Respiratory research · 2019Article
- Short-lived AUF1 p42-binding mRNAs of RANKL and BCL6 have two distinct instability elements each.PloS one · 2018Article
- Posttranscriptional Gene Regulation of T Follicular Helper Cells by RNA-Binding Proteins and microRNAs.Frontiers in immunology · 2018Review
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The expression of proteins during inflammatory and immune reactions is coordinated by post-transcriptional mechanisms. A particularly strong suppression of protein expression is exerted by a conserved translational silencing element (TSE) identified in the 3' UTR of NFKBIZ mRNA, which is among the targets of the RNA-binding proteins Roquin-1/2 and MCPIP1/Regnase-1. We present evidence that in the context of the TSE MCPIP1, so far known for its endonuclease activity toward mRNAs specified by distinct stem-loop (SL) structures, also suppresses translation. Overexpression of MCPIP1 silenced translation in a TSE-dependent manner and reduced ribosome occupancy of the mRNA. Correspondingly, MCPIP1 depletion alleviated silencing and increased polysomal association of the mRNA. Translationally silenced NFKBIZ or reporter mRNAs were mostly capped, polyadenylated and ribosome associated. Furthermore, MCPIP1 silenced also cap-independent, CrPV-IRES-dependent translation. This suggests that MCPIP1 suppresses a post-initiation step. The TSE is predicted to form five SL structures. SL4 and 5 resemble target structures reported for MCPIP1 and together were sufficient for MCPIP1 binding and mRNA destabilization. Translational silencing, however, required SL1-3 in addition. Thus the NFKBIZ TSE functions as an RNA element in which sequences adjacent to the site of interaction with MCPIP1 and dispensable for accelerated mRNA degradation extend the functional repertoire of MCPIP1 to translational silencing.
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