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Journal articles on the topic 'RNA interferent'

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Published: 4 June 2021
Last updated: 5 February 2022

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1

Tuschl, Thomas. "RNA Interference and Small Interfering RNAs." ChemBioChem 2, no. 4 (April 1, 2001): 239–45. http://dx.doi.org/10.1002/1439-7633(20010401)2:4<239::aid-cbic239>3.0.co;2-r.

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2

BENDER, Onur, Evrim ÇELEBİ, and Arzu ATALAY. "RNA Interference and Current Clinical Applications: Review." Turkiye Klinikleri Journal of Medical Sciences 36, no. 1 (2016): 53–60. http://dx.doi.org/10.5336/medsci.2015-49055.

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3

Poliseno, L., A. Mercatanti, L. Citti, and G. Rainaldi. "RNA-Based Drugs: From RNA Interference to Short Interfering RNAs." Current Pharmaceutical Biotechnology 5, no. 4 (August 1, 2004): 361–68. http://dx.doi.org/10.2174/1389201043376797.

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4

Jeon, Mi Jin, Mi Ja Seo, Young Nam Youn, and Yong Man Yu. "RNA Interference of Chitinase Gene in Spodoptera litura." Korean Journal of Pesticide Science 18, no. 3 (September 30, 2014): 202–9. http://dx.doi.org/10.7585/kjps.2014.18.3.202.

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5

Eberle, Florian, Kerstin Gießler, Christopher Deck, Klaus Heeg, Mirjam Peter, Clemens Richert, and Alexander H. Dalpke. "Modifications in Small Interfering RNA That Separate Immunostimulation from RNA Interference." Journal of Immunology 180, no. 5 (February 21, 2008): 3229–37. http://dx.doi.org/10.4049/jimmunol.180.5.3229.

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6

Sato, Fuminori, Tetsuto Nakagawa, Makoto Ito, Yasuo Kitagawa, and Masa-aki Hattori. "Application of RNA interference to chicken embryos using small interfering RNA." Journal of Experimental Zoology 301A, no. 10 (2004): 820–27. http://dx.doi.org/10.1002/jez.a.99.

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7

CAPLEN, NATASHA J., and SPYRO MOUSSES. "Short Interfering RNA (siRNA)-Mediated RNA Interference (RNAi) in Human Cells." Annals of the New York Academy of Sciences 1002, no. 1 (December 2003): 56–62. http://dx.doi.org/10.1196/annals.1281.007.

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8

Manoharan, Muthiah. "RNA interference and chemically modified small interfering RNAs." Current Opinion in Chemical Biology 8, no. 6 (December 2004): 570–79. http://dx.doi.org/10.1016/j.cbpa.2004.10.007.

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9

Duman-Scheel, Molly. "Saccharomyces cerevisiae (Baker’s Yeast) as an Interfering RNA Expression and Delivery System." Current Drug Targets 20, no. 9 (June 11, 2019): 942–52. http://dx.doi.org/10.2174/1389450120666181126123538.

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The broad application of RNA interference for disease prevention is dependent upon the production of dsRNA in an economically feasible, scalable, and sustainable fashion, as well as the identification of safe and effective methods for RNA delivery. Current research has sparked interest in the use of Saccharomyces cerevisiae for these applications. This review examines the potential for commercial development of yeast interfering RNA expression and delivery systems. S. cerevisiae is a genetic model organism that lacks a functional RNA interference system, which may make it an ideal system for expression and accumulation of high levels of recombinant interfering RNA. Moreover, recent studies in a variety of eukaryotic species suggest that this microbe may be an excellent and safe system for interfering RNA delivery. Key areas for further research and development include optimization of interfering RNA expression in S. cerevisiae, industrial-sized scaling of recombinant yeast cultures in which interfering RNA molecules are expressed, the development of methods for largescale drying of yeast that preserve interfering RNA integrity, and identification of encapsulating agents that promote yeast stability in various environmental conditions. The genetic tractability of S. cerevisiae and a long history of using this microbe in both the food and pharmaceutical industry will facilitate further development of this promising new technology, which has many potential applications of medical importance.
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10

Nykänen, Antti, Benjamin Haley, and Phillip D. Zamore. "ATP Requirements and Small Interfering RNA Structure in the RNA Interference Pathway." Cell 107, no. 3 (November 2001): 309–21. http://dx.doi.org/10.1016/s0092-8674(01)00547-5.

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11

Capodici, John, Katalin Karikó, and Drew Weissman. "Inhibition of HIV-1 Infection by Small Interfering RNA-Mediated RNA Interference." Journal of Immunology 169, no. 9 (November 1, 2002): 5196–201. http://dx.doi.org/10.4049/jimmunol.169.9.5196.

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12

Hall, Allison H. S., and Kenneth A. Alexander. "RNA Interference of Human Papillomavirus Type 18 E6 and E7 Induces Senescence in HeLa Cells." Journal of Virology 77, no. 10 (May 15, 2003): 6066–69. http://dx.doi.org/10.1128/jvi.77.10.6066-6069.2003.

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ABSTRACT The human papillomavirus oncoproteins E6 and E7 promote cell proliferation and contribute to carcinogenesis by interfering with the activities of cellular tumor suppressors. We used a small interfering RNA molecule targeting the E7 region of the bicistronic E6 and E7 mRNA to induce RNA interference, thereby reducing expression of E6 and E7 in HeLa cells. RNA interference of E6 and E7 also inhibited cellular DNA synthesis and induced morphological and biochemical changes characteristic of cellular senescence. These results demonstrate that reducing E6 and E7 expression is sufficient to cause HeLa cells to become senescent.
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13

Lebedev, T. D. "Specific silencing of leukemic oncogenes using RNA-interference approach." Ukrainian Biochemical Journal 85, no. 6 (December 27, 2013): 144–50. http://dx.doi.org/10.15407/ubj85.06.144.

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14

Halytskiy, V. A., and S. V. Komisarenko. "Specific silencing of leukemic oncogenes using RNA-interference approach." Ukrainian Biochemical Journal 85, no. 6 (December 27, 2013): 151–65. http://dx.doi.org/10.15407/ubj85.06.151.

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15

Liu, Tingting, Liping Wang, Hongchuan Xin, Lili Jin, and Dianbao Zhang. "Delivery Systems for RNA Interference-Based Therapy and Their Applications Against Cancer." Science of Advanced Materials 12, no. 1 (January 1, 2020): 75–86. http://dx.doi.org/10.1166/sam.2020.3694.

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RNA interference technology discovered in 1990 won the Nobel Prize in 2006. The first approved drug in 2018 inspired us once again. The technology has many advantages, but how to deliver it effectively has become a bottleneck to clinical practice. Lipid, polymer and modification methods have been developed to deliver small interfering RNA to target cells or tissues. Numerous clinical trials have been carried out to apply RNA interference technology to the treatment of tumors. This review covers the history and mechanism of RNA interference and the development of various delivery systems. The current progress of clinical trials for RNA interferencebased therapies against cancer is summarized. Challenges and opportunities for clinical application of RNA interference are discussed emphatically.
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16

Koper-Emde, Dorota, Lutz Herrmann, Björn Sandrock, and Bernd-Joachim Benecke. "RNA interference by small hairpin RNAs synthesised under control of the human 7S K RNA promoter." Biological Chemistry 385, no. 9 (September 1, 2004): 791–94. http://dx.doi.org/10.1515/bc.2004.103.

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AbstractSmall interfering RNAs (siRNAs) represent RNA duplexes of 21 nucleotides in length that inhibit gene expression. We have used the human gene-external 7S K RNA promoter for synthesis of short hairpin RNAs (shRNAs) which efficiently target human lamin mRNA via RNA interference (RNAi). Here we demonstrate that orientation of the target sequence within the shRNA construct is important for interference. Furthermore, effective interference also depends on the length and/or structure of the shRNA. Evidence is presented that the human 7S K promoter is more activein vivothan other gene-external promoters, such as the human U6 small nuclear RNA (snRNA) gene promoter.
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17

Ghosal, Anubrata, Ahmad Kabir, and Abul Mandal. "RNA interference and its therapeutic potential." Open Medicine 6, no. 2 (April 1, 2011): 137–47. http://dx.doi.org/10.2478/s11536-011-0005-5.

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AbstractRNA interference is a technique that has become popular in the past few years. This is a biological method to detect the activity of a specific gene within a cell. RNAi is the introduction of homologous double stranded RNA to specifically target a gene’s product resulting in null or hypomorphic phenotypes. This technique involves the degradation of specific mRNA by using small interfering RNA. Both microRNA (miRNA) and small interfering RNA (siRNA) are directly related to RNA interference. RNAi mechanism is being explored as a new technique for suppressing gene expression. It is an important issue in the treatment of various diseases. This review considers different aspects of RNAi technique including its history of discovery, molecular mechanism, gene expression study, advantages of this technique against previously used techniques, barrier associated with this technique, and its therapeutic application.
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18

Yu, Ji-wei, Shou-lian Wang, Ju-gang Wu, Rui-qi Lu, Xiao-chun Ni, Cheng Cai, and Bo-jian Jiang. "Study on the Biological Characteristics of CD133+ Cells Interfered by RNA Interference in Gastric Cancer." ISRN Gastroenterology 2014 (March 19, 2014): 1–11. http://dx.doi.org/10.1155/2014/329519.

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Background. To detect the changes of biological characteristics in gastric cancer cells interfered by CD133-specific small interfering RNA (siRNA). Methods. First to select the siRNA which has the strongest interference effect among 3 siRNAs (i.e., siRNA1, siRNA2, and siRNA3) in KATO-III cells by RT-PCR and Western blotting assays. Then, CD133+ cells were sorted out from KATO-III cells using an immunomagnetic bead sorting method and transfected with the selected siRNA. Furthermore, the proliferating characteristics, the antichemotherapeutic assessment, Transwell invasion assay, monoclonal sphere formation assay, and subcutaneous transplanted tumor formation assay in nude mice were investigated. Results. siRNA3 showed the strongest interference effect in KATO-III cells. As compared to the uninterfered control group, the CD133+ cells treated by siRNA3 showed significant decreases in the abilities of proliferation, invasion, clone sphere formation, and resistance to antitumour drugs as well as the weight and size of the transplanted tumor, which was nearly similar to that of CD133− cells. Additionally, the protein expression level of the EMT factor E-cadherin increased while those of EMT-related Snail and N-cadherin decreased in CD133+ cells interfered by siRNA3. Conclusion. Inhibition of CD133 gene expression reduces the abilities of gastric cancer cells in proliferation, invasion, clonal sphere formation, and chemoresistance as well as tumor formation in nude mice.
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19

Devers, Emanuel A., Christopher A. Brosnan, Alexis Sarazin, Daniele Albertini, Andrea C. Amsler, Florian Brioudes, Pauline E. Jullien, Peiqi Lim, Gregory Schott, and Olivier Voinnet. "Movement and differential consumption of short interfering RNA duplexes underlie mobile RNA interference." Nature Plants 6, no. 7 (July 2020): 789–99. http://dx.doi.org/10.1038/s41477-020-0687-2.

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20

Adamek, M., G. Rauch, G. Brogden, and D. Steinhagen. "Small interfering RNA treatment can inhibit Cyprinid herpesvirus 3 associated cell death in vitro." Polish Journal of Veterinary Sciences 17, no. 4 (December 1, 2014): 733–35. http://dx.doi.org/10.2478/pjvs-2014-0108.

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Abstract A Cyprinid herpesvirus 3 infection of carp induces a disease which causes substantial losses in carp culture. Here we present the use of a possible strategy for the management of the virus infection RNA interference based on small interfering RNAs. As a result of in vitro studies, we found that a mixture of short interfering RNAs specific for viral DNA enzyme synthesis and capsid proteins of the CyHV-3 can be a potential inhibitor of virus replication in fibroblastic cells. This gives the basis for the development of a combinatorial RNA interference strategy to treat CyHV-3 infections.
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21

Lin, Jennifer, and Bryan R. Cullen. "Analysis of the Interaction of Primate Retroviruses with the Human RNA Interference Machinery." Journal of Virology 81, no. 22 (September 12, 2007): 12218–26. http://dx.doi.org/10.1128/jvi.01390-07.

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ABSTRACT The question of whether retroviruses, including human immunodeficiency virus type 1 (HIV-1), interact with the cellular RNA interference machinery has been controversial. Here, we present data showing that neither HIV-1 nor human T-cell leukemia virus type 1 (HTLV-1) expresses significant levels of either small interfering RNAs or microRNAs in persistently infected T cells. We also demonstrate that the retroviral nuclear transcription factors HIV-1 Tat and HTLV-1 Tax, as well as the Tas transactivator encoded by primate foamy virus, fail to inhibit RNA interference in human cells. Moreover, the stable expression of physiological levels of HIV-1 Tat did not globally inhibit microRNA production or expression in infected human cells. Together, these data argue that HIV-1 and HTLV-1 neither induce the production of viral small interfering RNAs or microRNAs nor repress the cellular RNA interference machinery in infected cells.
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22

Lieberman, Judy, Erwei Song, Sang-Kyung Lee, and Premlata Shankar. "Interfering with disease: opportunities and roadblocks to harnessing RNA interference." Trends in Molecular Medicine 9, no. 9 (September 2003): 397–403. http://dx.doi.org/10.1016/s1471-4914(03)00143-6.

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23

Karagiannis, Tom C., and Assam El-Osta. "RNA interference and potential therapeutic applications of short interfering RNAs." Cancer Gene Therapy 12, no. 10 (May 13, 2005): 787–95. http://dx.doi.org/10.1038/sj.cgt.7700857.

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24

Gandhi, Sumit G., Indira Bag, Saswati Sengupta, Manika Pal-Bhadra, and Utpal Bhadra. "DrosophilaoncogeneGas41is an RNA interference modulator that intersects heterochromatin and the small interfering RNA pathway." FEBS Journal 282, no. 1 (November 17, 2014): 153–73. http://dx.doi.org/10.1111/febs.13115.

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25

Nakai, N., T. Kishida, M. Shin-Ya, J. Imanishi, Y. Ueda, S. Kishimoto, and O. Mazda. "Therapeutic RNA interference of malignant melanoma by electrotransfer of small interfering RNA targeting Mitf." Gene Therapy 14, no. 4 (October 5, 2006): 357–65. http://dx.doi.org/10.1038/sj.gt.3302868.

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26

Calegari, F., W. Haubensak, D. Yang, W. B. Huttner, and F. Buchholz. "Tissue-specific RNA interference in postimplantation mouse embryos with endoribonuclease-prepared short interfering RNA." Proceedings of the National Academy of Sciences 99, no. 22 (October 21, 2002): 14236–40. http://dx.doi.org/10.1073/pnas.192559699.

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27

Varley, Andrew J., and Jean-Paul Desaulniers. "Chemical strategies for strand selection in short-interfering RNAs." RSC Advances 11, no. 4 (2021): 2415–26. http://dx.doi.org/10.1039/d0ra07747j.

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28

Andersson, M. Gunnar, P. C. Joost Haasnoot, Ning Xu, Saideh Berenjian, Ben Berkhout, and Göran Akusjärvi. "Suppression of RNA Interference by Adenovirus Virus-Associated RNA." Journal of Virology 79, no. 15 (August 1, 2005): 9556–65. http://dx.doi.org/10.1128/jvi.79.15.9556-9565.2005.

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ABSTRACT We show that human adenovirus inhibits RNA interference (RNAi) at late times of infection by suppressing the activity of two key enzyme systems involved, Dicer and RNA-induced silencing complex (RISC). To define the mechanisms by which adenovirus blocks RNAi, we used a panel of mutant adenoviruses defective in virus-associated (VA) RNA expression. The results show that the virus-associated RNAs, VA RNAI and VA RNAII, function as suppressors of RNAi by interfering with the activity of Dicer. The VA RNAs bind Dicer and function as competitive substrates squelching Dicer. Further, we show that VA RNAI and VA RNAII are processed by Dicer, both in vitro and during a lytic infection, and that the resulting short interfering RNAs (siRNAs) are incorporated into active RISC. Dicer cleaves the terminal stem of both VA RNAI and VA RNAII. However, whereas both strands of the VA RNAI-specific siRNA are incorporated into RISC, the 3′ strand of the VA RNAII-specific siRNA is selectively incorporated during a lytic infection. In summary, our work shows that adenovirus suppresses RNAi during a lytic infection and gives insight into the mechanisms of RNAi suppression by VA RNA.
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29

Sledz, C. A., and B. R. G. Williams. "RNA interference and double-stranded-RNA-activated pathways." Biochemical Society Transactions 32, no. 6 (October 26, 2004): 952–56. http://dx.doi.org/10.1042/bst0320952.

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RNAi (RNA interference) has become a powerful tool to determine gene function. Different methods of expressing the short ds (double-stranded) RNA intermediates required for interference in mammalian systems have been developed, including the introduction of si (short interfering) RNAs by direct transfection or driven from transfected plasmids or lentiviral vectors encoding sh (short hairpin) RNAs. Although RNAi relies upon a high degree of specificity, recent findings suggest that off-target non-specific effects can be encountered. We found that transfection of siRNAs can results in an interferon-mediated activation of the JAK/STAT (Janus kinase/signal transducer and activator of transcription) pathway and global up-regulation of interferon-stimulated genes. This effect is mediated in part by the dsRNA-dependent protein kinase PKR, as this kinase is activated by the 21 bp siRNA, and is required in response to the siRNAs. However, the transcription factor IRF3 (interferon-regulatory factor 3) is also activated by siRNA as a primary response, resulting in the stimulation of genes independent of an interferon response. In cells deficient in IRF3, this response is blunted, but can be restored by re-introduction of IRF3. Thus siRNAs induce complex signalling responses in target cells, leading to effects beyond the selective silencing of specific genes.
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30

Lebedev, T. D., P. V. Spirin, and V. S. Prassolov. "Transfer and Expression of Small Interfering RNAs in Mammalian Cells Using Lentiviral Vectors." Acta Naturae 5, no. 2 (June 15, 2013): 7–18. http://dx.doi.org/10.32607/20758251-2013-5-2-7-18.

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RNA interference is a convenient tool for modulating gene expression. The widespread application of RNA interference is made difficult because of the imperfections of the methods used for efficient target cell delivery of whatever genes are under study. One of the most convenient and efficient gene transfer and expression systems is based on the use of lentiviral vectors, which direct the synthesis of small hairpin RNAs (shRNAs), the precursors of siRNAs. The application of these systems enables one to achieve sustainable and long-term shRNA expression in cells. This review considers the adaptation of the processing of artificial shRNA to the mechanisms used by cellular microRNAs and simultaneous expression of several shRNAs as potential approaches for producing lentiviral vectors that direct shRNA synthesis. Approaches to using RNA interference for the treatment of cancer, as well as hereditary and viral diseases, are under active development today. The improvement made to the methods for constructing lentiviral vectors and the investigation into the mechanisms of processing of small interfering RNA allow one to now consider lentiviral vectors that direct shRNA synthesis as one of the most promising tools for delivering small interfering RNAs.
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31

Ramon, Anne-Laure, Jean-Rémi Bertrand, and Claude Malvy. "Delivery of Small Interfering RNA. A Review and an Example of Application to a Junction Oncogene." Tumori Journal 94, no. 2 (March 2008): 254–63. http://dx.doi.org/10.1177/030089160809400218.

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RNA interference strategies using small interfering RNA is one of the most important discoveries in biology in recent years. This technology alongside antisense oligonucleotides is very promising and our group has focused its work on the targeting of junction oncogenes with these molecules. We have taken, as first example, papillary thyroid carcinoma. But there is a great need in delivery methods for these molecules in the treatment of cancers. Indeed, many studies have shown that small interfering RNA and antisense oligonucleotides are made efficient by various innovative delivery methods and, under these conditions, offer a powerful new therapeutic tool in cancer treatment.
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32

Shah, Samit, and Simon H. Friedman. "Tolerance of RNA Interference Toward Modifications of the 5′ Antisense Phosphate of Small Interfering RNA." Oligonucleotides 17, no. 1 (March 2007): 35–43. http://dx.doi.org/10.1089/oli.2006.0067.

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33

Sierant, Malgorzata, Julia Kazmierczak-Baranska, Alina Paduszynska, Milena Sobczak, Aleksandra Pietkiewicz, and Barbara Nawrot. "Longer 19-Base Pair Short Interfering RNA Duplexes Rather Than Shorter Duplexes Trigger RNA Interference." Oligonucleotides 20, no. 4 (August 2010): 199–206. http://dx.doi.org/10.1089/oli.2010.0239.

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34

Read, Martin L., Sohaib Mir, Rachel Spice, Ruth J. Seabright, Ellen L. Suggate, Zubair Ahmed, Martin Berry, and Ann Logan. "Profiling RNA interference (RNAi)-mediated toxicity in neural cultures for effective short interfering RNA design." Journal of Gene Medicine 11, no. 6 (June 2009): 523–34. http://dx.doi.org/10.1002/jgm.1321.

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35

Gitlin, Leonid, Jeffrey K. Stone, and Raul Andino. "Poliovirus Escape from RNA Interference: Short Interfering RNA-Target Recognition and Implications for Therapeutic Approaches." Journal of Virology 79, no. 2 (January 15, 2005): 1027–35. http://dx.doi.org/10.1128/jvi.79.2.1027-1035.2005.

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ABSTRACT Short interfering RNAs (siRNAs) directed against poliovirus and other viruses effectively inhibit viral replication. Although RNA interference (RNAi) may provide the basis for specific antiviral therapies, the limitations of RNAi antiviral strategies are ill defined. Here, we show that poliovirus readily escapes highly effective siRNAs through unique point mutations within the targeted regions. Competitive analysis of the escape mutants provides insights into the basis of siRNA recognition. The RNAi machinery can tolerate mismatches but is exquisitely sensitive to mutations within the central region and the 3′ end of the target sequence. Indeed, specific mutations in the target sequence resulting in G:U mismatches are sufficient for the virus to escape siRNA inhibition. However, using a pool of siRNAs to simultaneously target multiple sites in the viral genome prevents the emergence of resistant viruses. Our study uncovers the elegant precision of target recognition by the RNAi machinery and provides the basis for the development of effective RNAi-based therapies that prevent viral escape.
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36

Sweeney, B. P., and M. Z. Michel. "RNA interference." European Journal of Anaesthesiology 25, no. 7 (July 2008): 525–27. http://dx.doi.org/10.1017/s0265021508003992.

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37

ARNAUD, CELIA. "RNA INTERFERENCE." Chemical & Engineering News 84, no. 41 (October 9, 2006): 8. http://dx.doi.org/10.1021/cen-v084n041.p008.

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38

Downward, Julian. "RNA interference." BMJ 328, no. 7450 (May 20, 2004): 1245–48. http://dx.doi.org/10.1136/bmj.328.7450.1245.

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39

Pe'ery, T. "RNA interference." Methods 30, no. 4 (August 2003): 287–88. http://dx.doi.org/10.1016/s1046-2023(03)00035-5.

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40

FIGUEROA, BRYAN E., and ROBERT M. FRIEDLANDER. "RNA Interference." Neurosurgery 54, no. 3 (March 2004): NA. http://dx.doi.org/10.1227/01.neu.0000309606.99960.fd.

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41

Moyer, Paula. "RNA INTERFERENCE." Neurology Today 3, no. 7 (July 2003): 30–33. http://dx.doi.org/10.1097/00132985-200307000-00012.

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42

Sioud, Mouldy, and Abdelali Haoudi. "RNA Interference." Journal of Biomedicine and Biotechnology 2006 (2006): 1–2. http://dx.doi.org/10.1155/jbb/2006/89018.

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43

Eccleston, Alex, and Angela K. Eggleston. "RNA interference." Nature 431, no. 7006 (September 2004): 337. http://dx.doi.org/10.1038/431337a.

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44

Hannon, Gregory J. "RNA interference." Nature 418, no. 6894 (July 2002): 244–51. http://dx.doi.org/10.1038/418244a.

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45

Hoh, Yin Kiong. "RNA Interference." American Biology Teacher 76, no. 6 (August 1, 2014): 373–77. http://dx.doi.org/10.1525/abt.2014.76.6.4.

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46

Stallwood, Yvette. "RNA interference." Pharmacogenomics 6, no. 1 (January 2005): 13–16. http://dx.doi.org/10.1517/14622416.6.1.13.

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47

Russev, G. "RNA Interference." Biotechnology & Biotechnological Equipment 21, no. 3 (January 2007): 283–85. http://dx.doi.org/10.1080/13102818.2007.10817462.

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48

Lambeth, Luke S., Robert J. Moore, Morley S. Muralitharan, and Timothy J. Doran. "Suppression of bovine viral diarrhea virus replication by small interfering RNA and short hairpin RNA-mediated RNA interference." Veterinary Microbiology 119, no. 2-4 (January 2007): 132–43. http://dx.doi.org/10.1016/j.vetmic.2006.09.008.

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49

Kapadia, S. B., A. Brideau-Andersen, and F. V. Chisari. "Interference of hepatitis C virus RNA replication by short interfering RNAs." Proceedings of the National Academy of Sciences 100, no. 4 (February 3, 2003): 2014–18. http://dx.doi.org/10.1073/pnas.252783999.

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50

Best, Alexander, Lusy Handoko, Elke Schlüter, and H. U. Göringer. "In VitroSynthesized Small Interfering RNAs Elicit RNA Interference in African Trypanosomes." Journal of Biological Chemistry 280, no. 21 (March 21, 2005): 20573–79. http://dx.doi.org/10.1074/jbc.m414534200.

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