ArticleNucleic acids research2012
Increased in vivo inhibition of gene expression by combining RNA interference and U1 inhibition.
Article in Nucleic acids research, 2012. 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, 17 citations in OpenAlex.
- Circ-find-0001774 Modulates Parkinson's Disease via miR-153-3p: Mechanistic Insights and Therapeutic Implications.Journal of molecular neuroscience : MN · 2026Article
- Potentiation of anti-angiogenic eNOS-siRNA transfection by ultrasound-mediated microbubble destruction in ex vivo rat aortic rings.PloS one · 2024Article
- U1A is a positive regulator of the expression of heterologous and cellular genes involved in cell proliferation and migration.Molecular therapy. Nucleic acids · 2022Article
- ISR8/IRF1-AS1 Is Relevant for IFNα and NF-κB Responses.Frontiers in immunology · 2022Article
- Emerging Roles of RNA 3'-end Cleavage and Polyadenylation in Pathogenesis, Diagnosis and Therapy of Human Disorders.Biomolecules · 2020Review
- Nucleotide Modifications Decrease Innate Immune Response Induced by Synthetic Analogs of snRNAs and snoRNAs.Genes · 2018Article
- Long noncoding RNA EGOT negatively affects the antiviral response and favors HCV replication.EMBO reports · 2016Article
- Therapeutic activity of modified U1 core spliceosomal particles.Nature communications · 2016Article
- Long Non-Coding RNA BST2/BISPR is Induced by IFN and Regulates the Expression of the Antiviral Factor Tetherin.Frontiers in immunology · 2014Article
- Alternative polyadenylation of tumor suppressor genes in small intestinal neuroendocrine tumors.Frontiers in endocrinology · 2014Article
- Alterations in polyadenylation and its implications for endocrine disease.Frontiers in endocrinology · 2013Article
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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
Inhibition of gene expression can be achieved with RNA interference (RNAi) or U1 small nuclear RNA-snRNA-interference (U1i). U1i is based on U1 inhibitors (U1in), U1 snRNA molecules modified to inhibit polyadenylation of a target pre-mRNA. In culture, we have shown that the combination of RNAi and U1i results in stronger inhibition of reporter or endogenous genes than that obtained using either of the techniques alone. We have now used these techniques to inhibit gene expression in mice. We show that U1ins can induce strong inhibition of the expression of target genes in vivo. Furthermore, combining U1i and RNAi results in synergistic inhibitions also in mice. This is shown for the inhibition of hepatitis B virus (HBV) sequences or endogenous Notch1. Surprisingly, inhibition obtained by combining a U1in and a RNAi mediator is higher than that obtained by combining two U1ins or two RNAi mediators. Our results suggest that RNAi and U1i cooperate by unknown mechanisms to result in synergistic inhibitions. Analysis of toxicity and specificity indicates that expression of U1i inhibitors is safe. Therefore, we believe that the combination of RNAi and U1i will be a good option to block damaging endogenous genes, HBV and other infectious agents in vivo.
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Registered trials
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