ArticleScientific reports2015
The hematopoietic regulator, ELF-1, enhances the transcriptional response to Interferon-β of the OAS1 anti-viral gene.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 20 citations in OpenAlex.
- Gouty inflammation: genetic mechanisms towards flare therapy.Current opinion in rheumatology · 2025Review
- CXXC5 is a ubiquitinated protein and is degraded by the ubiquitin-proteasome pathway.Protein science : a publication of the Protein Society · 2025Article
- Elf1 Deficiency Impairs Macrophage Development in Zebrafish Model Organism.International journal of molecular sciences · 2025Article
- ELF1 suppresses autophagy to reduce cisplatin resistance via the miR-152-3p/NCAM1/ERK axis in lung cancer cells.Cancer science · 2023Article
- An integrated analysis of the cancer genome atlas data discovers a hierarchical association structure across thirty three cancer types.PLOS digital health · 2022Article
- Bioinformatics and systems-biology analysis to determine the effects of Coronavirus disease 2019 on patients with allergic asthma.Frontiers in immunology · 2022Article
- A CpG island promoter drives the CXXC5 gene expression.Scientific reports · 2021Article
- The Immune-Related Gene ELF3 is a Novel Biomarker for the Prognosis of Ovarian Cancer.International journal of general medicine · 2021Article
- The ETS transcription factor ELF1 regulates a broadly antiviral program distinct from the type I interferon response.PLoS pathogens · 2019Article
- The accessible chromatin landscape of the murine hippocampus at single-cell resolution.Genome research · 2019Article
- Characterization of the 5'-flanking region of the human DNA helicase B (HELB) gene and its response to trans-Resveratrol.Scientific reports · 2016Article
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Authors and funding
4 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Interferon (IFN) therapy is effective in treating cancers, haematological and virus induced diseases. The classical Jak/Stat pathway of IFN signal transduction leading to changes in transcriptional activity is well established but alone does not explain the whole spectrum of cellular responses to IFN. Gene promoters contain cis-acting sequences that allow precise and contextual binding of transcription factors, which control gene expression. Using the transcriptional response to IFN as a starting point we report a high frequency of tandem GGAA motifs in the proximal promoters of Interferon stimulated genes, suggesting a key regulatory action. Utilizing the well-characterized anti-viral gene, OAS1, as an example Interferon stimulated gene promoter containing such a duplicated GGAA motif, we have demonstrated a regulatory role of this promoter in response to IFN by mutation analysis. Furthermore, we identified ELF-1 as a direct binding factor at this motif. Additionally, recruitment of RB1 and SP1 factors to the promoter following IFN stimulation is shown. ELF-1 overexpression enhanced and knockdown of ELF-1 inhibited full activation of OAS1 by IFN stimulation. Collectively, ELF-1 binds an important duplicated GGAA cis-acting element at the OAS1 promoter and in cooperation with RB1 and SP1 recruitment contributes to regulation in response to IFN stimulation.
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