ArticleFrontiers in immunology2014
Regulation of Interferon-Stimulated Gene BST2 by a lncRNA Transcribed from a Shared Bidirectional Promoter.
Article in Frontiers in immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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46 citing papers in PubMed, 62 citations in OpenAlex.
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- An integrative atlas of chicken long non-coding genes and their annotations across 25 tissues.Scientific reports · 2020Article
- LncRNA and mRNA expression profile of peripheral blood mononuclear cells in primary Sjögren's syndrome patients.Scientific reports · 2020Article
- LncRNAs in the Type I Interferon Antiviral Response.International journal of molecular sciences · 2020Review
- Novel Mechanism of Microvesicle Regulation by the Antiviral Protein Tetherin During HIV Infection.Journal of the American Heart Association · 2020Article
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- The impact of bone marrow stromal antigen-2 (BST2) gene variants on HIV-1 control in black South African individuals.Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases · 2020Article
- LncRNAs in HCV Infection and HCV-Related Liver Disease.International journal of molecular sciences · 2020Review
- Long non-coding RNA RP11-468E2.5 curtails colorectal cancer cell proliferation and stimulates apoptosis via the JAK/STAT signaling pathway by targeting STAT5 and STAT6.Journal of experimental & clinical cancer research : CR · 2019Article
- Long non-coding RNA PSMB8-AS1 regulates influenza virus replication.RNA biology · 2019Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Recent genome-wide studies have revealed the presence of thousands of long non-protein-coding RNAs (lncRNAs), some of which may play critical roles in the cell. We have previously shown that a large number of lncRNAs show differential expression in response to interferon (IFN)α stimulation in primary human cells. Here, we show that a subset of IFN-induced lncRNAs are positioned in proximity of protein-coding IFN-stimulated genes (ISGs). The majority of gene pairs originated from bidirectional promoters and showed positively correlated expression. We focused our analysis on a pair consisting of the known protein-coding ISG, BST2, and an un-studied putative lncRNA originating from the promoter region of BST2 in a divergent orientation. We showed that this transcript was a multi-exonic, polyadenylated long RNA that lacked protein-coding capacity. BST2 and the lncRNA were both induced in response to IFNα in diverse cell types. The induction of both genes was mediated through the JAK-STAT pathway, suggesting that IFN-stimulated response elements within the shared promoter activated the transcription of both genes. RNAi-mediated knock-down of the lncRNA resulted in down-regulation of BST2, and we could show that this down-regulation occurred at the level of transcription. Forced overexpression of this lncRNA, which we named BST2 IFN-Stimulated Positive Regulator (BISPR), resulted in up-regulation of BST2, indicating that the regulation of expression of BST2 by BISPR is mediated through interactions involving BISPR RNA itself, rather than the impact of its transcription from an adjacent locus. Importantly, upon IFN stimulation, transcriptional activation of BISPR preceded the induction of BST2, suggesting that expression of BISPR facilitated the initiation of transcription in its paired protein-coding gene. The lncRNA-mediated transcriptional regulation described in this study may help govern the expression of additional protein-coding RNAs involved in IFN response and other cellular processes.
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