Готові списки джерел за темами / Morpholino Oligomers

Добірка наукової літератури з теми "Morpholino Oligomers"

Автор: Grafiati

Опубліковано: 7 вересня 2023

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Статті в журналах з теми "Morpholino Oligomers"

Aung-Htut, May T., Craig S. McIntosh, Kristin A. West, Sue Fletcher, and Steve D. Wilton. "In Vitro Validation of Phosphorodiamidate Morpholino Oligomers." Molecules 24, no. 16 (August 12, 2019): 2922. http://dx.doi.org/10.3390/molecules24162922.

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One of the crucial aspects of screening antisense oligonucleotides destined for therapeutic application is confidence that the antisense oligomer is delivered efficiently into cultured cells. Efficient delivery is particularly vital for antisense phosphorodiamidate morpholino oligomers, which have a neutral backbone, and are known to show poor gymnotic uptake. Here, we report several methods to deliver these oligomers into cultured cells. Although 4D-Nucleofector™ or Neon™ electroporation systems provide efficient delivery and use lower amounts of phosphorodiamidate morpholino oligomer, both systems are costly. We show that some readily available transfection reagents can be used to deliver phosphorodiamidate morpholino oligomers as efficiently as the electroporation systems. Among the transfection reagents tested, we recommend Lipofectamine 3000™ for delivering phosphorodiamidate morpholino oligomers into fibroblasts and Lipofectamine 3000™ or Lipofectamine 2000™ for myoblasts/myotubes. We also provide optimal programs for nucleofection into various cell lines using the P3 Primary Cell 4D-Nucleofector™ X Kit (Lonza), as well as antisense oligomers that redirect expression of ubiquitously expressed genes that may be used as positive treatments for human and murine cell transfections.

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Neuman, Benjamin W., David A. Stein, Andrew D. Kroeker, Amy D. Paulino, Hong M. Moulton, Patrick L. Iversen, and Michael J. Buchmeier. "Antisense Morpholino-Oligomers Directed against the 5′ End of the Genome Inhibit Coronavirus Proliferation and Growth†." Journal of Virology 78, no. 11 (June 1, 2004): 5891–99. http://dx.doi.org/10.1128/jvi.78.11.5891-5899.2004.

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ABSTRACT Conjugation of a peptide related to the human immunodeficiency virus type 1 Tat represents a novel method for delivery of antisense morpholino-oligomers. Conjugated and unconjugated oligomers were tested to determine sequence-specific antiviral efficacy against a member of the Coronaviridae, Mouse hepatitis virus (MHV). Specific antisense activity designed to block translation of the viral replicase polyprotein was first confirmed by reduction of luciferase expression from a target sequence-containing reporter construct in both cell-free and transfected cell culture assays. Peptide-conjugated morpholino-oligomers exhibited low toxicity in DBT astrocytoma cells used for culturing MHV. Oligomer administered at micromolar concentrations was delivered to >80% of cells and inhibited virus titers 10- to 100-fold in a sequence-specific and dose-responsive manner. In addition, targeted viral protein synthesis, plaque diameter, and cytopathic effect were significantly reduced. Inhibition of virus infectivity by peptide-conjugated morpholino was comparable to the antiviral activity of the aminoglycoside hygromycin B used at a concentration fivefold higher than the oligomer. These results suggest that this composition of antisense compound has therapeutic potential for control of coronavirus infection.

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McIntosh, Craig S., May Thandar Aung-Htut, Sue Fletcher, and Steve D. Wilton. "Removal of the Polyglutamine Repeat of Ataxin-3 by Redirecting pre-mRNA Processing." International Journal of Molecular Sciences 20, no. 21 (October 31, 2019): 5434. http://dx.doi.org/10.3390/ijms20215434.

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Spinocerebellar ataxia type 3 (SCA3) is a devastating neurodegenerative disease for which there is currently no cure, nor effective treatment strategy. One of nine polyglutamine disorders known to date, SCA3 is clinically heterogeneous and the main feature is progressive ataxia, which in turn affects speech, balance and gait of the affected individual. SCA3 is caused by an expanded polyglutamine tract in the ataxin-3 protein, resulting in conformational changes that lead to toxic gain of function. The expanded glutamine tract is located at the 5′ end of the penultimate exon (exon 10) of ATXN3 gene transcript. Other studies reported removal of the expanded glutamine tract using splice switching antisense oligonucleotides. Here, we describe improved efficiency in the removal of the toxic polyglutamine tract of ataxin-3 in vitro using phosphorodiamidate morpholino oligomers, when compared to antisense oligonucleotides composed of 2′-O-methyl modified bases on a phosphorothioate backbone. Significant downregulation of both the expanded and non-expanded protein was induced by the morpholino antisense oligomer, with a greater proportion of ataxin-3 protein missing the polyglutamine tract. With growing concerns over toxicity associated with long-term administration of phosphorothioate oligonucleotides, the use of a phosphorodiamidate morpholino oligomer may be preferable for clinical application. These results suggest that morpholino oligomers may provide greater therapeutic benefit for the treatment of spinocerebellar ataxia type 3, without toxic effects.

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Burgess, Darren J. "Targeting huntingtin through morpholino oligomers." Nature Reviews Genetics 15, no. 9 (August 12, 2014): 572. http://dx.doi.org/10.1038/nrg3804.

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Summerton, James, and Dwight Weller. "Antisense Properties of Morpholino Oligomers." Nucleosides and Nucleotides 16, no. 7-9 (July 1997): 889–98. http://dx.doi.org/10.1080/07328319708006105.

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Iversen, Patrick, Katherine Aird, Rebecca Wu, Michael Morse, and Gayathri Devi. "Cellular Uptake of Neutral Phosphorodiamidate Morpholino Oligomers." Current Pharmaceutical Biotechnology 10, no. 6 (September 1, 2009): 579–88. http://dx.doi.org/10.2174/138920109789069279.

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SUMMERTON, JAMES, and DWIGHT WELLER. "Morpholino Antisense Oligomers: Design, Preparation, and Properties." Antisense and Nucleic Acid Drug Development 7, no. 3 (June 1997): 187–95. http://dx.doi.org/10.1089/oli.1.1997.7.187.

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Puckett, Susan E., Kaleb A. Reese, Georgi M. Mitev, Valerie Mullen, Rudd C. Johnson, Kyle R. Pomraning, Brett L. Mellbye, et al. "Bacterial Resistance to Antisense Peptide Phosphorodiamidate Morpholino Oligomers." Antimicrobial Agents and Chemotherapy 56, no. 12 (September 17, 2012): 6147–53. http://dx.doi.org/10.1128/aac.00850-12.

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ABSTRACTPeptide phosphorodiamidate morpholino oligomers (PPMOs) are synthetic DNA mimics that bind cRNA and inhibit bacterial gene expression. The PPMO (RFF)3RXB-AcpP (where R is arginine, F, phenylalanine, X is 6-aminohexanoic acid, B is β-alanine, and AcpP is acyl carrier protein) is complementary to 11 bases of the essential geneacpP(which encodes acyl carrier protein). The MIC of (RFF)3RXB-AcpP was 2.5 μM (14 μg/ml) inEscherichia coliW3110. The rate of spontaneous resistance ofE. colito (RFF)3RXB-AcpP was 4 × 10−7mutations/cell division. A spontaneous (RFF)3RXB-AcpP-resistant mutant (PR200.1) was isolated. The MIC of (RFF)3RXB-AcpP was 40 μM (224 μg/ml) for PR200.1. The MICs of standard antibiotics for PR200.1 and W3110 were identical. The sequence ofacpPwas identical in PR200.1 and W3110. PR200.1 was also resistant to other PPMOs conjugated to (RFF)3RXB or peptides with a similar composition or pattern of cationic and nonpolar residues. Genomic sequencing of PR200.1 identified a mutation insbmA, which encodes an active transport protein. In separate experiments, a (RFF)3RXB-AcpP-resistant isolate (RR3) was selected from a transposome library, and the insertion was mapped tosbmA. Genetic complementation of PR200.1 or RR3 withsbmArestored susceptibility to (RFF)3RXB-AcpP. Deletion ofsbmAcaused resistance to (RFF)3RXB-AcpP. We conclude that resistance to (RFF)3RXB-AcpP was linked to the peptide and not the phosphorodiamidate morpholino oligomer, dependent on the composition or repeating pattern of amino acids, and caused by mutations insbmA. The data further suggest that (RFF)3R-XB PPMOs may be transported across the plasma membrane by SbmA.

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Ham, Kristin A., May Thandar Aung-Htut, Sue Fletcher, and Steve D. Wilton. "Nonsequential Splicing Events Alter Antisense-Mediated Exon Skipping Outcome in COL7A1." International Journal of Molecular Sciences 21, no. 20 (October 18, 2020): 7705. http://dx.doi.org/10.3390/ijms21207705.

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The COL7A1 gene encodes homotrimer fibrils essential for anchoring dermal and epidermal layers, and pathogenic mutations in COL7A1 can cause recessive or dominant dystrophic epidermolysis bullosa. As a monogenic disease gene, COL7A1 constitutes a potential target for antisense oligomer-mediated exon skipping, a therapy applicable to a growing number of other genetic disorders. However, certain characteristics of COL7A1: many exons, low average intron size, and repetitive and guanine-cytosine rich coding sequence, present challenges to the design of specific and effective antisense oligomers. While targeting COL7A1 exons 10 and 73 for excision from the mature mRNA, we discovered that antisense oligomers comprised of 2′-O-methyl modified bases on a phosphorothioate backbone and phosphorodiamidate morpholino oligomers produced similar, but distinctive, splicing patterns including excision of adjacent nontargeted exons and/or retention of nearby introns in some transcripts. We found that the nonsequential splicing of certain introns may alter pre-mRNA processing during antisense oligomer-mediated exon skipping and, therefore, additional studies are required to determine if the order of intron removal influences multiexon skipping and/or intron retention in processing of the COL7A1 pre-mRNA.

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HUDZIAK, ROBERT M., ELISABETH BAROFSKY, DOUGLAS F. BAROFSKY, DOREEN L. WELLER, SUNG-BEN HUANG, and DWIGHT D. WELLER. "Resistance of Morpholino Phosphorodiamidate Oligomers to Enzymatic Degradation." Antisense and Nucleic Acid Drug Development 6, no. 4 (January 1996): 267–72. http://dx.doi.org/10.1089/oli.1.1996.6.267.

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Більше джерел

Дисертації з теми "Morpholino Oligomers"

Han, Xue. "Inhibition of PRRSV replication by combination of antisense morpholino oligomers." College Park, Md.: University of Maryland, 2008. http://hdl.handle.net/1903/8633.

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Thesis (M.S.) -- University of Maryland, College Park, 2008.
Thesis research directed by: Dept. of Animal and Avian Sciences. Title from t.p. of PDF. Includes bibliographical references. Published by UMI Dissertation Services, Ann Arbor, Mich. Also available in paper.

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Ramirez, A. "PEPTIDE-CONJUGATED MORPHOLINO OLIGOMERS FOR TREATMENT OF SPINAL MUSCULAR ATROPHY." Doctoral thesis, Università degli Studi di Milano, 2018. http://hdl.handle.net/2434/541107.

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Spinal muscular atrophy (SMA) is an autosomal recessive motor neuron disease and the first known genetic cause of infant mortality. It is caused by the homozygous mutations in the Survival Motor Neuron 1 (SMN1) gene, resulting in deficiency of functional SMN protein. The pathologic aspect of SMA is the progressive loss of Motor Neurons (MNs) in the ventral horn of the spinal cord, which causes the loss of muscle function, paralysis and premature death. A first drug for SMA, Nusinersen an antisense oligonucleotide (ASO) has been recently been approved. In fact, one of the most promising strategies in order to increase the SMN protein levels is the use of ASOs to redirect the splicing of the paralogous gene SMN2 to increase the production of the functional SMN protein. ASOs with different chemical structure are currently used in clinical trials, included the ASO with Morpholino (MO) chemistry studied in this work. MO oligomers are particularly suitable for in vivo applications thanks to their optimal safety and efficacy profile. One of the issues related to the administration of ASOs is that they are not able to cross the blood-brain barrier and they must be administered by relatively invasive intrathecal injection to reach the central nervous system (CNS). Therefore, we aimed to improve the efficacy of MO and to develop a non-invasive systemic delivery in an in vivo SMA murine model. First, to increase the efficacy of MO oligomers, we tested, both in vitro and in vivo, four new MO sequences targeting the region involved in the alternative splicing of SMN2 mRNA, called intronic splicing silencer N1 (ISS-N1). Simultaneously, to improve the delivery of MO to affected tissues, we conjugated it to cell-penetrating peptides (CPPs), an approach already used to enhance the cellular and tissue uptake and the pharmacological profile of ASOs, but never explored in SMA. We tested three different CPPs: Tat, R6, and (RXRRBR)2XB, which were linked to our already validated MO sequence [HSMN2Ex7D(-10,-34)]. We administered the conjugates in pre-symptomatic and symptomatic SMA mice to determine their therapeutic efficacy versus unconjugated-MO. We showed that optimization of the target sequence can enhance the splice-correction action of MO oligomers and that the effect of the co-administration of different MO sequences is superior to the delivery of a single sequence. Furthermore, we showed that CPP-MO compounds can up-regulate the SMN protein into the CNS of SMA7 transgenic murine models as well as their average lifespan and motor performance after local and systemic injection. Our data proved that the CPP-MO conjugates can be a suitable strategy to increase the cellular uptake after an intrathecal administration and to deliver MO oligomers to the CNS after a systemic injection. The presented results provided the basis for the selection of the most efficient CPPs and will set the stage for future clinical trials.

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Biayna, Rodríguez Josep. "Using Phosphorodiamidate Morpholino Oligomers (PMOs) to characterize the role of neurofibromin in cell physiology." Doctoral thesis, Universitat de Barcelona, 2016. http://hdl.handle.net/10803/378358.

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The role of neurofibromin, the product of the Neurofibromatosis Type 1 (NF1) gene, in cell physiology is still not well understood. Considering the different traits associated to NF1 it is clear that neurofibromin participates in processes of proliferation and differentiation of different cell types. The Ras-GAP activity of neurofibromin is its best characterized biochemical function, which is regulated by the alternative splicing of exon 23a (E23a). In this thesis we intended to better understand the role of alternative splicing of E23a during neuronal differentiation, with the aim that in the future it could provide information on the learning and cognitive issues related to this disease. Due to the large size of neurofibromin, the difficulty of manipulating it in vitro and the necessity to mimic, as much as possible, the physiological conditions of the cell, we used Phosphorodiamidate Morpholino Oligomers (PMOs) to modify the exonic composition of NF1 mRNA while preserving the endogenous neurofibromin expression levels. We developed a PMO-based system that successfully allowed to force the expression of type II (+E23a) or type I (-E23a) isoforms without altering the physiological expression levels of NF1 mRNA in PC12 cells, a neuronal differentiation model, in the presence or absence of Nerve Growth Factor (NGF). This PMO system could be used in other cellular models of NF1, and could be reproduced for studying the regulation of the alternative splicing in other genes. Furthermore, we set up a group of functional assays for assessing proliferation, differentiation, signaling and apoptosis in this PC12 neuronal model. Our results showed that forcing type I (-E23a) isoform was not sufficient for inducing PC12 neuronal differentiation in the absence of NGF. However, the results also demonstrate that any alteration of the NGF-induced ratio between type I/II isoforms, either in a quantitative or time-dependent manner, interfered with the correct neuronal differentiation process, in particular, altering the correct formation of neurites, as well as the proper regulation of the RAS/MAPK and cAMP/PKA signalling pathways. Moreover, the alteration of the natural E23a alternative splicing also impeded the proper neuronal differentiation process in other neuronal models, such as the H19-7 hippocampus cells. Our results also showed that the depletion of neurofibromin in PC12 induce a generalized process of apoptosis; suggest the existence of an early negative feed-back on the function of neurofibromin when type I isoform is abnormally expressed, and shows that the regulation of the cAMP/PKA pathway is also dependent on the GAP domain of neurofibromin. All together, the results of this thesis indicate that the regulation of the alternative splicing of exon 23a of the NF1 gene allows the fine-tuning of the RAS/MAPK and cAMP/PKA pathways through its GAP activity in a coordinate and opposite way along the time-dependent process of neuronal differentiation.
La neurofibromina és el producte del gen NF1, que mutat causa la Neurofibromatosis de tipus 1. Tot i que en l'actualitat, encara ens cal entendre millor el rol d'aquesta proteïna en la fisiologia cel•lular, l'activitat Ras-GAP és la funció bioquímica més ben caracteritzada de la neurofibromina. Aquesta funció està regulada per l'splicing alternatiu de l'exó 23a (E23a). En aquesta tesi ens vàrem proposar comprendre millor el paper d'aquest splicing alternatiu durant el procés de diferenciació neuronal, amb l'objectiu de proporcionar nova informació sobre els problemes cognitius i d'aprenentatge associats a aquesta malaltia. Degut a la gran grandària de la neurofibromina i a la dificultat de manipular-la in vitxo, es varen utilitzar Phosphorodiamidate Morpholino Oligomers (PMOs) per modificar la composició exònica del mARN (per tant l'estructura resultant de la neurofibromina) sense alterar les condicions fisiològiques d'expressió del gen NF 1 . Es va desenvolupar un sistema basat en PMOs per forçar l'expressió de l'isoforma tipus II (+E23a) o tipus I (-E23a) del gen NF1 en cèl•lules PC12, un model de diferenciació neuronal, en presència o absència de Nerve Growth Factor (NGF). A més, per entendre la importància de 1'E23a es va establir un grup de metodologies i assajos funcionals per poder determinar diferents respostes cel•lulars i valorar la funció d'aquest en el procés de diferenciació neuronal. Els nostres resultats van mostrar que forçar l'isoforma tipus I (-E23a) no era suficient per induir la diferenciació de les cèl•lules PC12 en absència de NGF. No obstant això, qualsevol alteració en la relació entre les isoformes tipus I/II en presència de NGF, ja sigui d'una manera quantitativa o dependent del temps, interferia en el correcte procés de diferenciació neuronal, en particular, alterant la correcta formació de neurites, així com l'adequada regulació de les vies de senyalització RAS/MAPK i cAMP/PKA. En conjunt, els resultats d'aquesta tesi indiquen que la regulació de l'splicing alternatiu de 1'E23a del gen NF1 permet un ajust fi de les vies RAS/MAPK i cAMP/PKA a través de la activitat GAP de la neurofibromina, d'una forma oposada i coordinada al llarg del temps durant el procés de diferenciació neuronal.

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Simmons, Tabatha Renee. "Treatment of DMD 5’ Mutations through Two Different Exon 2 Skipping Strategies: rAAV9.U7snRNA Mediated Skipping and Antisense Morpholino Oligomers." The Ohio State University, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=osu1469122227.

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Kang, Jagjeet Kaur. "Antisense-mediated myostatin downregulation by destructive exon skipping using 2'O-methyl RNA and morpholino oligomers in skeletal muscle cells and animal products." Thesis, University of London, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.589410.

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Myostatin is a negative regulator of muscle mass, and several strategies are being developed to knock down the expression of the myostatin gene as a means to bring about improvements in muscle wasting conditions, including Duchenne muscular dystrophy (DMD). Improved muscle regeneration in the absence of myostatin has been demonstrated in mdx mice by-crossing them with myostatin null mice. Increased muscle strength and improved dystrophic pathophysiology has been found in the mdx mice treated with myostatin antibodies, purified myostatin propeptide (natural binding partner of myostatin) with a mouse fusion protein and AA V -mediated transfer of propeptide. Virus-based strategies have the major drawbacks of uncontrolled insertion into the target genome and undesirable immune response; whereas, injecting binding partners to the target-tissue might have low sustainability over a longer period of time. In this study the design and use of anti sense oligonucleotides (AOs) to manipulate myostatin pre-mRNA splicing and knockdown myostatin has been described. AOs of both 2'O-methyl RNA (2'OMePS-with a phosphorothioate backbone) and phosphorodiarnidate morpholino (PMO) chemistries were designed using different bioinformatics algorithms. Efficiency of destructive myostatin exon skipping was then demonstrated and evaluated comparatively by oligomer transfection of cultured muscle cells, and RT-PCR and bioactivity analyses. Sustained and high levels of destructive exon skipping of the myostatin mRNA, and increases in skeletal muscle mass and fibre sizes was observed up toi months following a single injection of Vivo-PMO (PMO conjugated to a cell-penetrating octa-guanidine moiety) into the tibialis anterior muscle in normal mice. The efficiency of Vivo-PMO was also compared to a PMO conjugated to a cell penetrating peptide moiety (B-PMO) by single intra -muscular treatment of wild type mice. Weekly intravenous injections of Vivo- PMO in normal mice also lead to myostatin exon skipping in selected skeletal muscles, and associated increases in tissue mass, cross-sectional area, and average fibre diameter. Dual exon skipping of myostatin and dystrophin was also carried out successfully in mdx mice. These studies indicate that (i) anti sense-mediated destructive exon skipping can be induced in the myostatin RNA, (ii) anti sense AO treatment reduces myostatin bioactivity and enhances muscle mass in vivo, and (iii) AO-induced myostatin exon- skipping may be a potential therapeutic strategy to counter muscular dystrophy, muscular atrophy, cachexia and sarcopenia.

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Книги з теми "Morpholino Oligomers"

Moulton, Hong M., and Jon D. Moulton, eds. Morpholino Oligomers. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-6817-6.

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Morpholino Oligomers: Methods and Protocols. Springer New York, 2017.

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Moulton, Hong M., and Jon D. Moulton. Morpholino Oligomers: Methods and Protocols. Springer New York, 2018.

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Частини книг з теми "Morpholino Oligomers"

Summerton, James E. "Invention and Early History of Morpholinos: From Pipe Dream to Practical Products." In Morpholino Oligomers, 1–15. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-6817-6_1.

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Daly, Seth M., Carolyn R. Sturge, and David E. Greenberg. "Inhibition of Bacterial Growth by Peptide-Conjugated Morpholino Oligomers." In Morpholino Oligomers, 115–22. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-6817-6_10.

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Krtková, Jana, and Alexander R. Paredez. "Use of Translation Blocking Morpholinos for Gene Knockdown in Giardia lamblia." In Morpholino Oligomers, 123–40. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-6817-6_11.

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Gong, Qiuming, and Zhengfeng Zhou. "Regulation of Isoform Expression by Blocking Polyadenylation Signal Sequences with Morpholinos." In Morpholino Oligomers, 141–50. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-6817-6_12.

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Crossley, Madzia P., and Torsten Krude. "Targeting Functional Noncoding RNAs." In Morpholino Oligomers, 151–60. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-6817-6_13.

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Liu, Guozheng. "Use of Morpholino Oligomers for Pretargeting." In Morpholino Oligomers, 161–79. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-6817-6_14.

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Levicky, Rastislav, Ursula Koniges, and Napoleon Tercero. "Diagnostic Applications of Morpholinos and Label-Free Electrochemical Detection of Nucleic Acids." In Morpholino Oligomers, 181–90. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-6817-6_15.

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Rajsbaum, Ricardo. "Intranasal Delivery of Peptide-Morpholinos to Knockdown Influenza Host Factors in Mice." In Morpholino Oligomers, 191–99. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-6817-6_16.

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Maruyama, Rika, Yusuke Echigoya, Oana Caluseriu, Yoshitsugu Aoki, Shin’ichi Takeda, and Toshifumi Yokota. "Systemic Delivery of Morpholinos to Skip Multiple Exons in a Dog Model of Duchenne Muscular Dystrophy." In Morpholino Oligomers, 201–13. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-6817-6_17.

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Karunakaran, Devi Krishna Priya, and Rahul Kanadia. "In Vivo and Explant Electroporation of Morpholinos in the Developing Mouse Retina." In Morpholino Oligomers, 215–27. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-6817-6_18.

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Тези доповідей конференцій з теми "Morpholino Oligomers"

Jiang, Shan. "Abstract 715: Vivo-Morpholino antisense oligomers decrease tumor growth in mice by altering mVEGF mRNA splicing to knock down mVEGF expression." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-715.

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