ArticleFEBS open bio2019
TRIM14 expression is regulated by IRF-1 and IRF-2.
Article in FEBS open bio, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
5 citing papers in PubMed, 17 citations in OpenAlex.
- Emerging discoveries on the role of TRIM14: from diseases to immune regulation.Cell death discovery · 2024Review
- LncRNA GAS6-AS1 facilitates tumorigenesis and metastasis of colorectal cancer by regulating TRIM14 through miR-370-3p/miR-1296-5p and FUS.Journal of translational medicine · 2022Article
- Article
- Cytosolic DNA sensing by cGAS: regulation, function, and human diseases.Signal transduction and targeted therapy · 2021Review
- To TRIM or not to TRIM: the balance of host-virus interactions mediated by the ubiquitin system.The Journal of general virology · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tripartite motif-containing 14 (TRIM14) is a mitochondrial adaptor that promotes innate immune signaling and plays important roles in antiviral defense. Expression of TRIM14 is induced by interferon (IFN)-I. However, the mechanism by which IFN-I induces TRIM14 production is not yet determined. In this study, we have examined the function of TRIM14 promoter and found that a GC box and an IFN-stimulated response element (ISRE) are necessary for the basal level transcription of TRIM14. We further observed that IFN-I activates the TRIM14 promoter through the ISRE. In particular, interferon regulatory factor (IRF)-1 and IRF-2 bind to the TRIM14 promoter and activate transcription of TRIM14. Moreover, knockdown of IRF-1 reduces the stimulation of TRIM14 transcription by IFN-α, suggesting that IRF-1 is involved in the activation of TRIM14 by IFN-I. IRF-2 has little effect on IFN-α-induced TRIM14 transcription but is essential for the basal transcription of TRIM14.
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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.