ArticleRNA (New York, N.Y.)2007
A more efficient RNAi inducible system for tight regulation of gene expression in mammalian cells and xenograft animals.
Article in RNA (New York, N.Y.), 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 27 citations in OpenAlex.
- Overexpression of AKR1C3 significantly enhances human prostate cancer cells resistance to radiation.Oncotarget · 2016Article
- Persistence of RNAi-Mediated Knockdown in Drosophila Complicates Mosaic Analysis Yet Enables Highly Sensitive Lineage Tracing.Genetics · 2016Article
- A plant alkaloid, veratridine, potentiates cancer chemosensitivity by UBXN2A-dependent inhibition of an oncoprotein, mortalin-2.Oncotarget · 2015Article
- Systematic transfer of prokaryotic sensors and circuits to mammalian cells.ACS synthetic biology · 2014Article
- Elevated expression of AKR1C3 increases resistance of cancer cells to ionizing radiation via modulation of oxidative stress.PloS one · 2014Article
- Development of a multipurpose GATEWAY-based lentiviral tetracycline-regulated conditional RNAi system (GLTR).PloS one · 2014Article
- c-Met targeting enhances the effect of irradiation and chemical agents against malignant colon cells harboring a KRAS mutation.PloS one · 2014Article
- Transferring a synthetic gene circuit from yeast to mammalian cells.Nature communications · 2013Article
- Strand antagonism in RNAi: an explanation of differences in potency between intracellularly expressed siRNA and shRNA.Nucleic acids research · 2012Article
- The construction of siRNA plasmid targeting mouse HIF-1alpha and in vitro study of its inhibition effect.Neuroscience bulletin · 2009Article
- A method for detecting and preventing negative RNA interference in preparation of lentiviral vectors for siRNA delivery.RNA (New York, N.Y.) · 2009Article
- Modeling recursive RNA interference.PLoS computational biology · 2008Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Two types of tetracycline-controlled inducible RNAi expression systems have been developed that generally utilize multiple tetracycline operators (TetOs) or repressor fusion proteins to overcome the siRNA leakiness. Here, we report a novel system that overexpresses the tetracycline repressor (TetR) via a bicistronic construct to control siRNA expression. The high level of TetR expression ensures that the inducible promoter is tightly bound, with minimal basal transcription, allowing for regulation solely dependent on TetR rather than a TetR fusion protein via a more complicated mechanism. At the same time, this system contains only a single TetO, thus minimizing the promoter impairment occurring in existing systems due to the incorporation of multiple TetOs, and maximizing the siRNA expression upon induction. In addition, this system combines all the components required for regulation of siRNA expression into a single lentiviral vector, so that stable cell lines can be generated by a single transduction and selection, with significant reduction in time and cost. Taken together, this all-in-one lentiviral vector with the feature of TetR overexpression provides a unique and more efficient tool for conditional gene knockdown that has wide applications. We have demonstrated the high degree of robustness and versatility of this system as applied to several mammalian cells and xenograft animals.
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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.