ArticlePloS one2016
TRIB1 Is Regulated Post-Transcriptionally by Proteasomal and Non-Proteasomal Pathways.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
18 citing papers in PubMed, 25 citations in OpenAlex.
- Rapid increase of C/EBPα p42 induces growth arrest of acute myeloid leukemia (AML) cells by Cop1 deletion in Trib1-expressing AML.Leukemia · 2024Article
- Review
- Loss of Pip4k2c confers liver-metastatic organotropism through insulin-dependent PI3K-AKT pathway activation.Nature cancer · 2024Article
- Article
- Regulation of TRIB1 abundance in hepatocyte models in response to proteasome inhibition.Scientific reports · 2023Article
- Unraveling molecular characteristic of fluoride neurotoxicity on U87 glial-like cells: insights from transcriptomic and proteomic approach.Frontiers in cellular neuroscience · 2023Article
- Review
- Comprehensive Profiling of Mammalian Tribbles Interactomes Implicates TRIB3 in Gene Repression.Cancers · 2021Article
- Self-Organizing Human Induced Pluripotent Stem Cell Hepatocyte 3D Organoids Inform the Biology of the PleiotropicHepatology communications · 2020Article
- Tribbles-1 Expression and Its Function to Control Inflammatory Cytokines, Including Interleukin-8 Levels are Regulated by miRNAs in Macrophages and Prostate Cancer Cells.Frontiers in immunology · 2020Article
- 2018 George Lyman Duff Memorial Lecture: Genetics and Genomics of Coronary Artery Disease: A Decade of Progress.Arteriosclerosis, thrombosis, and vascular biology · 2019Article
- TRIB1 rs17321515 gene polymorphism increases the risk of coronary heart disease in general population and non-alcoholic fatty liver disease patients in Chinese Han population.Lipids in health and disease · 2019Article
- The pseudokinase TRIB1 toggles an intramolecular switch to regulate COP1 nuclear export.The EMBO journal · 2019Article
- Pleiotropic mapping and annotation selection in genome-wide association studies with penalized Gaussian mixture models.Bioinformatics (Oxford, England) · 2018Article
- TRIB1 is a positive regulator of hepatocyte nuclear factor 4-alpha.Scientific reports · 2017Article
- Tribbles in the 21st Century: The Evolving Roles of Tribbles Pseudokinases in Biology and Disease.Trends in cell biology · 2017Review
- The Oncogenic Role of Tribbles 1 in Hepatocellular Carcinoma Is Mediated by a Feedback Loop Involving microRNA-23a and p53.Frontiers in physiology · 2017Article
- Human TRIB2 Oscillates during the Cell Cycle and Promotes Ubiquitination and Degradation of CDC25C.International journal of molecular sciences · 2016Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The TRIB1 gene has been associated with multiple malignancies, plasma triglycerides and coronary artery disease (CAD). Despite the clinical significance of this pseudo-kinase, there is little information on the regulation of TRIB1. Previous studies reported TRIB1 mRNA to be unstable, hinting that TRIB1 might be subject to post-transcriptional regulation. This work explores TRIB1 regulation, focusing on its post-transcriptional aspects. In 3 distinct model systems (HEK293T, HeLa and arterial smooth muscle cells) TRIB1 was undetectable as assessed by western blot. Using recombinant TRIB1 as a proxy, we demonstrate TRIB1 to be highly unstable at the protein and RNA levels. By contrast, recombinant TRIB1 was stable in cellular extracts. Blocking proteasome function led to increased protein steady state levels but failed to rescue protein instability, demonstrating that the 2 processes are uncoupled. Unlike as shown for TRIB2, CUL1 and TRCPβ did not play a role in mediating TRIB1 instability although TRCPβ suppression increased TRIB1 expression. Lastly, we demonstrate that protein instability is independent of TRIB1 subcellular localization. Following the identification of TRIB1 nuclear localization signal, a cytosolic form was engineered. Despite being confined to the cytosol, TRIB1 remained unstable, suggesting that instability occurs at a stage that precedes its nuclear translocation and downstream nuclear function. These results uncover possible avenues of intervention to regulate TRIB1 function by identifying two distinct regulatory axes that control TRIB1 at the post-transcriptional level.
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Registered trials
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.