ArticleThe Journal of biological chemistry2009
RNA-destabilizing factor tristetraprolin negatively regulates NF-kappaB signaling.
Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.
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Who cites it
62 citing papers in PubMed, 89 citations in OpenAlex.
- Improving Dietary Intake of Essential Nutrients Can Ameliorate Inflammation in Patients with Diabetic Foot Ulcers.Nutrients · 2022Trial
- The ZFP36 Family as a Post-Transcriptional Immune Checkpoint in Immunity and Disease: Molecular Mechanisms and Functional Implications.Biomolecules · 2026Review
- Endothelin-1 induces Zfp36 family RNA-binding proteins and restrains cytokine and chemokine production in reactive astrocytes.The Journal of biological chemistry · 2026Article
- Article
- ZFP36L1 and ZFP36L2 reduce cyclin D1 expression by decreasing expression of E2F1 and long 3'UTR isoform of CCND1 transcripts.Molecular and cellular biochemistry · 2025Article
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- Re-Exploring the Inflammation-Related Core Genes and Modules in Cerebral Ischemia.Molecular neurobiology · 2023Article
- Review
- AU-Rich Element RNA Binding Proteins: At the Crossroads of Post-Transcriptional Regulation and Genome Integrity.International journal of molecular sciences · 2021Review
- Inhibitory feedback control of NF-κB signalling in health and disease.The Biochemical journal · 2021Review
- ZFP36 protects lungs from intestinal I/R-induced injury and fibrosis through the CREBBP/p53/p21/Bax pathway.Cell death & disease · 2021Article
- Zinc finger proteins: insights into the transcriptional and post transcriptional regulation of immune response.Molecular biology reports · 2021Review
- Tristetraprolin Gene Single-Nucleotide Polymorphisms and mRNA Level in Patients With Rheumatoid Arthritis.Frontiers in pharmacology · 2021Article
- Promoter Methylation Leads to DecreasedFrontiers in medicine · 2020Article
- Network-Based Approach to Identify the Antiproliferative Mechanisms of Bruceine D in Breast Cancer From the Cancer Genome Atlas.Frontiers in oncology · 2020Article
- [Tristetraprolin inhibits autophagy in cultured lung cancer cellsNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2019Article
- Low Tristetraprolin Expression Is Associated with Lethal Prostate Cancer.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2019Article
- Roles of Tristetraprolin in Tumorigenesis.International journal of molecular sciences · 2018Review
- Myeloid-specific deletion of Zfp36 protects against insulin resistance and fatty liver in diet-induced obese mice.American journal of physiology. Endocrinology and metabolism · 2018Article
- A Knock-In Tristetraprolin (TTP) Zinc Finger Point Mutation in Mice: Comparison with Complete TTP Deficiency.Molecular and cellular biology · 2018Article
2 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tristetraprolin (TTP) is a CCCH zinc finger-containing protein that destabilizes mRNA by binding to an AU-rich element. Mice deficient in TTP develop a severe inflammatory syndrome mainly because of overproduction of tumor necrosis factor alpha. We report here that TTP also negatively regulates NF-kappaB signaling at the transcriptional corepressor level, by which it may repress inflammatory gene transcription. TTP expression inhibited NF-kappaB-dependent transcription. However, overexpression of TTP did not affect reporter mRNA stability. Instead, TTP functioned as a corepressor of p65/NF-kappaB. In support of this concept, we found that TTP physically interacted with the p65 subunit of NF-kappaB and was also associated with HDAC1, -3, and -7 in vivo. Treatment with histone deacetylase inhibitors or small interfering RNA induced HDAC1 or HDAC3 knockdown completely or partly abolished the inhibitory activity of TTP on NF-kappaB reporter activation. Consistently, chromatin immunoprecipitation showed decreased recruitment of HDAC1 and increased recruitment of CREB-binding protein on the Mcp-1 promoter in TTP(-/-) cells compared with wild-type cells. Moreover, overexpression of TTP blocked CREB-binding protein-induced acetylation of p65/NF-kappaB. Taken together, these data suggest that TTP may also function in vivo as a modulator in suppressing the transcriptional activity of NF-kappaB.
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