Bibliografías temáticas / Antisense RNA

Literatura académica sobre el tema "Antisense RNA"

Autor: Grafiati

Publicado: 4 de junio de 2021

Última modificación: 30 de julio de 2024

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Artículos de revistas sobre el tema "Antisense RNA"

Eguchi, Yutaka, Tateo Itoh y Jun-ichi Tomizawa. "Antisense RNA". Annual Review of Biochemistry 60, n.º 1 (junio de 1991): 631–52. http://dx.doi.org/10.1146/annurev.bi.60.070191.003215.

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Weitzman, Jonathan B. "Antisense RNA". Genome Biology 3 (2002): spotlight—20020125–01. http://dx.doi.org/10.1186/gb-spotlight-20020125-01.

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PESTKA, SIDNEY. "Antisense RNA." Annals of the New York Academy of Sciences 660, n.º 1 (octubre de 1992): 251–62. http://dx.doi.org/10.1111/j.1749-6632.1992.tb21077.x.

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Nordström, Kurt. "Antisense RNA". Trends in Biochemical Sciences 10, n.º 6 (junio de 1985): 232. http://dx.doi.org/10.1016/0968-0004(85)90138-0.

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Lacombe, Julie, Ekaterina Viazovkina, Pascal N. Bernatchez, Annie Galarneau, Masad J. Damha y Martin G. Sirois. "Antisense inhibition of Flk-1 by oligonucleotides composed of 2'-deoxy-2'-fluoro-β-D-arabino- and 2'-deoxy-nucleosides". Canadian Journal of Physiology and Pharmacology 80, n.º 10 (1 de octubre de 2002): 951–61. http://dx.doi.org/10.1139/y02-123.

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The design of new antisense oligomers with improved binding affinity for targeted RNA, while still activating RNase H, is a major research area in medicinal chemistry. RNase H recognizes the RNADNA duplex and cleaves the complementary mRNA strand, providing the main mechanism by which antisense oligomers elicit their activities. It has been shown that configuration inversion at the C2' position of the DNA sugar moiety (arabinonucleic acid, ANA), combined with the substitution of the 2'OH group by a fluorine atom (2' F-ANA) increases the oligomer's binding affinity for targeted RNA. In the present study, we evaluated the antisense activity of mixed-backbone phosphorothioate oligomers composed of 2'-deoxy-2'-fluoro-β-D-arabinose and 2'-deoxyribose sugars (S-2' F-ANADNA chimeras). We determined their abilities to inhibit the protein expression and phosphorylation of Flk-1, a vascular endothelial growth factor receptor (VEGF), and VEGF biological effects on endothelial cell proliferation, migration, and platelet-activating factor synthesis. Treatment of endothelial cells with chimeric oligonucleotides reduced Flk-1 protein expression and phosphorylation more efficiently than with phosphorothioate antisenses (S-DNA). Nonetheless, these two classes of antisenses inhibited VEGF activities equally. Herein, we also demonstrated the capacity of the chimeric oligomers to elicit RNase H activity and their improved binding affinity for complementary RNA as compared with S-DNA.Key words: antisense DNA, 2' F-ANA nucleosides, mixed-backbone antisense, Flk-1, VEGF.

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TURGUT, Kenan. "Antisense RNA Technology". Turkish Journal of Agriculture and Forestry 20, n.º 5 (1 de enero de 1996): 455–58. http://dx.doi.org/10.55730/1300-011x.2897.

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Liu, Zhong y Gordon G. Carmichael. "Nuclear antisense RNA". Molecular Biotechnology 2, n.º 2 (octubre de 1994): 107–18. http://dx.doi.org/10.1007/bf02824803.

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Brantl, Sabine. "Antisense-RNA regulation and RNA interference". Biochimica et Biophysica Acta (BBA) - Gene Structure and Expression 1575, n.º 1-3 (mayo de 2002): 15–25. http://dx.doi.org/10.1016/s0167-4781(02)00280-4.

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Werner, Andreas. "Natural Antisense Transcripts". RNA Biology 2, n.º 2 (abril de 2005): 53–62. http://dx.doi.org/10.4161/rna.2.2.1852.

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Funato, Tadao, Mayu Takeda y Mami Yoshida. "World of antisense RNA." SEIBUTSU BUTSURI KAGAKU 51, n.º 3 (2007): 207–9. http://dx.doi.org/10.2198/sbk.51.207.

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Tesis sobre el tema "Antisense RNA"

Tanniche, Imen. "Correlating antisense RNA performance with thermodynamic calculations". Thesis, Virginia Tech, 2013. http://hdl.handle.net/10919/49698.

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Antisense RNA (asRNA) strategies are identified as an effective and specific method for gene down-regulation at the post-transcriptional level. In this study, the major purpose is to find a correlation between the expression level and minimum free energy to enable the design of specific asRNA fragments. The thermodynamics of asRNA and mRNA hybridization were computed based on the fluorescent protein reporter genes. Three different fluorescent proteins (i) green fluorescent protein (GFP), (ii) cyan fluorescent protein (CFP) and (iii) yellow fluorescent protein (YFP) were used as reporters. Each fluorescent protein was cloned into the common pUC19 vector. The asRNA fragments were randomly amplified and the resulted antisense DNA fragments were inserted into the constructed plasmid under the control of an additional inducible plac promoter and terminator. The expression levels of fluorescent reporter protein were determined in real time by plate reader. Different results have been observed according to the fluorescent protein and the antisense fragment sequence. The CFP expression level was decreased by 50 to 78% compared to the control. However, with the GFP, the down-regulation did not exceed 30% for the different constructs used. For certain constructs, the effect was the opposite of expected and the expression level was increased. In addition, the YFP showed a weak signal compared to growth media, therefore the expression level was hard to be defined. Based on these results, a thermodynamic model to describe the relationship between the particular asRNA used and the observed expression level of the fluorescent reporter was developed. The minimum free energy and binding percentage of asRNA-mRNA complex were computed by NUPACK software. The expression level was drawn as a function of the minimum free energy. The results showed a weak correlation, but linear trends were observed for low energy values and low expression levels the CFP gene. The linear aspect is not verified for higher energy values. These findings suggest that the lower the energy is, the more stable is the complex asRNA-mRNA and therefore more reduction of the expression is obtained. Meanwhile, the non-linearity involves that there are other parameters to be investigated to improve the mathematical correlation. This model is expected to offer the chance to "fine-tune" asRNA effectiveness and subsequently modulate gene expression and redirect metabolic pathways toward the desired component. In addition, the investigation of the localization of antisense binding indicates that there are some regions that favors the hybridization and promote hence the down-regulation mechanisms.
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Denoeux, Stanislas. "Etude de la régulation de l'expression des gènes par un ARN antisens". Thesis, Université Paris-Saclay (ComUE), 2015. http://www.theses.fr/2015SACLS167/document.

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Au cours de la dernière décennie, les avancées du séquençage à haut débit ont permis de caractériser un grand nombre d’ARN non codant et d’établir l’existence de transcrits “antisens” pour de nombreux gènes chez les mammifères. Cependant leur rôle dans le contrôle de l’expression des gènes “sens” auxquels ils sont associés est encore très mal connu. Mes travaux ont porté sur la caractérisation de certains aspects du mécanisme d’action des longs ARN non codants. Ils reposent sur le développement d’une approche de constructions indicatrices fluorescentes dont l’expression est suivie par cytométrie en flux en présence ou non d’ARN “antisens”. Cette approche a le potentiel de mettre en évidence une régulation même si elle n’est présente que dans une sous population cellulaire. Une première série d’expériences a été réalisée en expression transitoire pour bénéficier d’un contexte chromatinien simplifié. Mais dans ce cas les silencing observés sont aussi actifs sur une construction contrôle, indiquant la mise en place d’une réponse non spécifique de séquence qui évoque la réponse de type interféron. Cependant, l’expression globale des gènes cellulaire n’est pas significativement affectée, indiquant une certaine spécificité de la réponse. Parmi les voies testées ni la kinase PKR, ni la RNaseL ou la voie de l’interférence par l’ARN ne peuvent rendre compte du silencing observé. Une des caractéristiques de cette régulation est qu’elle n’affecte pas les gènes intégrés au génome mais uniquement les gènes exprimés à partir d’une construction épisomale ce qui évoque des caractéristiques souhaitables pour un mécanisme antiviral. Cependant l’ampleur de cette réponse non spécifique empêche toute étude plus approfondie d’un mécanisme spécifique s’il existe. Mes travaux se sont alors portés sur l’étude de ces mêmes constructions en clone stable dans deux contextes différents pour l’expression de l’ARN antisens ; en cis ou en trans. Dans le cas de l’expression en trans, un ARN antisens sans séquence régulatrice particulière ne permet pas la mise en place d’un silencing. Cette observation est en accord avec le faible nombre de longs ARN antisens connus pour agir en trans dans la nature. Par contre l’expression en cis d’un ARN antisens peut conduire à un silencing spécifique. Cette organisation dans laquelle les gènes « sens » et « antisens » sont situés sur le même fragment d’ADN correspond à celle majoritairement observée pour les longs ARNs antisens dans la nature (cisNAT, cis Natural Antisense Transcripts). Cependant, mes travaux montrent que le silencing observé n’est pas stable dans le temps et disparaît dès lors que la transcription antisens cesse, indiquant l’absence d’une mémoire épigénétique. Un tel mode de régulation est compatible avec une interférence transcriptionnelle dans laquelle la transcription et non le produit ARN est la cause du silencing. Par ailleurs, j’ai observé un certain nombre de cas de co-régulation du transcrit sens et antisens ce qui traduit la possibilité d’activer en cis la transcription du gène cible par le promoteur de son ARN antisens. Ce phénomène est probablement facilité par la petite taille de nos constructions, mais cette dualité de réponse est en accord avec l’absence de corrélation (positive ou négative) entre l’expression des gènes et de leur transcrits antisens. L’ensemble de mes travaux montrent la faible capacité d’un ARN antisens à induire un silencing. L’approche développée doit donc permettre de rechercher des co-activateurs du silencing, par exemple en introduisant des sites de recrutement de complexes modificateurs de la chromatine
During the last decade next generation sequencing has allowed the characterization of a large number of non-coding RNA and to establish that a majority of mammalian genes were also transcribed in the opposite orientation. However the functional significance of this antisense transcription is currently unclear.My work focused on the characterization of the regulatory potential of long non-coding RNA. It relied on the use of fluorescent reporter constructs, the expression of which in the presence or absence of antisense RNA is analyzed by flow cytometry. . This approach has the potential to uncover a regulation mechanism even if it takes place only in a subpopulation of cells.A first series of experiments has been realized by transient expression assays in order to benefit from a simplified chromatin context. However in this case the silencing associated with antisense transcripts is also active on control constructs, indicating that at least part of the response is not sequence specific suggesting the involvement of an interferon-type response. However, cellular gene expression is not significantly affected indicating some level of specificity. Among the investigated pathways, neither the PKR kinase, nor RNaseL or RNA interference pathway can account for the observed silencing. One of this regulation attributes is that it does not affect genes integrated in the genome but only genes expressed from episomes, a selectivity which would seem appropriate for an antiviral mechanism. Nevertheless the extent of this non-specific response impedes any further study on a specific mechanism, if it operates.My work then focused on the study of these reporter constructs after integration in the genome, antisense RNA being expressed in cis or in trans.In the case of trans expression, an antisense RNA devoid of any specific regulatory sequence does not allow the setting of a silencing. This observation is consistent with the low number of long antisense RNA known to act in trans in nature.On the other side, the cis expression of an antisense RNA can lead to a specific silencing. This organization in which “sense” and “antisense” genes are located in the same DNA fragment matches with the ones mostly observed for long antisense RNA in nature (cisNAT, cis Natural Antisense Transcripts). However, my work shows that the observed silencing is not stable over time and the effects terminate once antisense transcription stops, which indicates the absence of an epigenetic memory. This mode of regulation is compatible with a transcriptional interference in which transcription – and not its RNA product - is causing the silencing. Besides, I observed a certain number of sense and antisense transcript co-regulation cases highlighting the possibility to activate the transcription of the target gene by the promoter of its antisense RNA. This phenomenon is probably facilitated by the small size of our constructs, but this duality of response is in agreement with the lack of correlation (either positive or negative) between the expression of genes and their antisense transcripts.This study shows the limited capacity of an antisense RNA to induce a silencing. The developed approach should allow the search for silencing co-activators, for instance by introducing chromatin remodeling complexes recruitment sites

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Faridani, Omid Reza. "Studies on natural antisense RNAs and microRNAs /". Stockholm : Karolinska institutet, 2007. http://diss.kib.ki.se/2007/978-91-7357-412-9/.

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Raponi, Mitch Biochemistry &amp Molecular Genetics UNSW. "Antisense RNA-mediated gene silencing in fission yeast". Awarded by:University of New South Wales. Biochemistry and Molecular Genetics, 2001. http://handle.unsw.edu.au/1959.4/18277.

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The major aims of this thesis were to investigate the influence of i) antisense gene location relative to the target gene locus (?????location effect?????), ii) double-stranded RNA (dsRNA) formation, and iii) over-expression of host-encoded proteins on antisense RNA-mediated gene regulation. To test the location effect hypothesis, strains were generated which contained the target lacZ gene at a fixed location and the antisense lacZ gene at various genomic locations including all arms of the three fission yeast chomosomes and in close proximity to the target gene locus. A long inverse-PCR protocol was developed to rapidly identify the precise site of antisense gene integration in the fission yeast transformants. No significant difference in lacZ suppression was observed when the antisense gene was integrated in close proximity to the target gene locus, compared with other genomic locations, indicating that target and antisense gene co-localisation is not a critical factor for efficient antisense RNA-mediated gene suppression in vivo. Instead, increased lacZ down-regulation correlated with an increase in the steady-state level of antisense RNA, which was dependent on genomic position effects and transgene copy number. In contrast, convergent transcription of an overlapping antisense lacZ gene was found to be very effective at inhibiting lacZ gene expression. DsRNA was also found to be a central component of antisense RNA-mediated gene silencing in fission yeast. It was shown that gene suppression could be enhanced by increasing the intracellular concentration of non-coding lacZ RNA, while expression of a lacZ panhandle RNA also inhibited beta-galactosidase activity. In addition, over-expression of the ATP-dependent RNA-helicase, ded1, was found to specifically enhance antisense RNA-mediated gene silencing. Through a unique overexpression screen, four novel factors were identified which specifically enhanced antisense RNA-mediated gene silencing by up to an additional 50%. The products of these antisense enhancing sequences (aes factors), all have natural associations with nucleic acids which is consistent with other proteins which have previously been identified to be involved in posttranscriptional gene silencing.

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Tan, Felicia. "Characterization of pilE antisense RNA in Neisseria meningitidis". Thesis, University of Oxford, 2016. https://ora.ox.ac.uk/objects/uuid:23d8f4c4-b423-4638-986b-b6b8e3fe95ec.

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Expression of Type four pili is important for colonization and virulence in Neisseria meningitidis, which is a major causative agent of bacterial meningitis and septicaemia. Pili mediate adhesion, twitching motility, DNA uptake, and can be subject to phase and antigenic variation (Av). Pilin expression and Av may be modulated in response to environmental cues; however, the mechanisms of regulation are still unclear. This work demonstrates the identification of a novel cis-encoded RNA on the antisense (AS) strand of pilE, which encodes the major pilin subunit. The AS promoter is conserved in different N. meningitidis isolates, suggesting that the AS RNA may play an important role N. meningitidis biology. By Northern blot and strand-specific qRT-PCR, the AS transcript was shown to be expressed during specific conditions, namely after overnight growth and in response to salt stress. The AS RNA was found to encompass sequences antisense to the entire pilE coding sequence and 5' untranslated region, and extends to a promoter upstream of pilE that drives expression of a G4 small RNA that is important for pilin Av. Noncoding RNAs are increasingly recognized as important regulators of gene expression in bacteria. AS RNAs often modulate expression of the sense mRNA, however in this study, overexpression or deletion of the AS RNA had no significant effect on pilE transcript or pilin levels despite its long stretch of complementarity to the pilE mRNA. Potential trans targets were also investigated by performing RNAseq analysis to identify differentially expressed genes in the absence of the AS RNA. Expression of the AS RNA was found to reduce the frequency of pilE variation. The possible influence of the AS RNA on G4 small RNA transcription was investigated by examining its effect on the levels of G4 small RNA and RNA:DNA hybrids. Although technical issues prevented us from obtaining definitive results, our findings suggest the AS RNA forms RNA:DNA hybrids, adding an additional layer of complexity of molecular processes in the pilE locus of N. meningitidis.

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Mitrpant, Chalermchai. "Pre-mRNA splicing manipulation via Antisense Oligomers". Thesis, Edith Cowan University, Research Online, Perth, Western Australia, 2009. https://ro.ecu.edu.au/theses/421.

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Duchenne muscular dystrophy (DMD), the most common lethal neuromuscular disease in childhood, arises from protein-truncating mutations in the dystrophin gene. A deficiency in dystrophin leads to loss of the dystrophin associated protein complex (DAPC), which in turn, renders muscle fibres vulnerable to injury, and eventually leads to muscle loss, necrosis and fibrosis. Although, the dystrophin gene was identified nearly two decades ago, and extensive research has been directed at finding a therapy for DMD, to date, there is still no effective treatment available. One promising molecular approach to treat DNID is antisense oligomer (AO) induced splice intervention. AOs were most widely used to induce RNaseH-mediated gene transcript degradation, however, the development of different backbone chemistries heralds a new generation of AOs that can modify gene transcript splicing patterns. Application of AOs to the dystrophin pre-mRNA to influence exon selection and induce shortened, in-frame dystrophin isoforms is being vigorously pursued. The majority of the work presented here explores the concept of personalised therapies for DMD, whereby oligomers are designed to specifically target individual mutations. The importance of AO-optimisation to obtain AOs capable of inducing efficient dual exon skipping in an established animal model of muscular dystrophy (4CV mouse), which carries a DMD-causing mutation in exon 53, is demonstrated. Removal of both exons 52 and 53 was required to by-pass the mutation, maintain the reading frame and restore dystrophin expression. One of the major challenges of AO-induced splice intervention for therapeutic purposes will be the design and development of clinically relevant oligomers for many different mutations. Various models, including cells transfected with artificial constructs and mice carrying a human dystrophin transgene, have been proposed as tools to facilitate oligomer design for splice manipulation. This thesis investigates the relevance of using mouse models to design AOs for human application, and also explores the use of cultured human myoblasts, from both unaffected humans and a DMD patient, as a means of establishing the most effective therapeutic compound. In addition to induction of exon skipping, the applicability of AOs to promote exon inclusion, by masking possible intronic silencing motifs of survival motor neuron (SMN) pre-mRNA in cultured fibroblasts from a spinal muscular atrophy (SMA) patient, is investigated. This study provides additional information about a novel oligomer target site that could be used in combination with previously identified splice silencing motifs for a molecular therapeutic approach to SMA, and may perhaps open up new avenues of treatment for other genetic disorders, where oIigomers could be used to induce exon inclusion.

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Reimegård, Johan. "Making Sense of Antisense". Doctoral thesis, Uppsala universitet, Mikrobiologi, 2010. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-131168.

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RNA is a highly versatile molecule with functions that span from being a messenger in the transfer from DNA to protein, a catalytic molecule important for key processes in the cell to a regulator of gene expression. The post-genomic era and the use of new techniques to sequence RNAs have dramatically increased the number of regulatory RNAs during the last decade. Many of these are antisense RNAs, as for example the miRNA in eukaryotes and most sRNAs in bacteria. Antisense RNAs bind to specific targets by basepairing and thereby regulate their expression. A major step towards an understanding of the biological role of a miRNA or an sRNA is taken when one identifies which target it regulates. We have used RNA libraries to study the RNA interference pathway during development in the unicellular model organism Dictyostelium discoideum. We have also, by combining computational and experimental methods, discovered the first miRNAs in this organism and shown that they have different expression profiles during development. In parallel, we have developed a novel approach to predict targets for sRNAs in bacteria and used it to discover sRNA/target RNA interactions in the model organism Escherichia coli. We have found evidence for, and further characterized, three of these predicted sRNA/target interactions. For instance, the sRNA MicA is important for regulation of the outer membrane protein OmpA, the sRNAs OmrA and OmrB regulate the transcription factor CsgD, which is important in the sessile lifestyle of E. coli, and MicF regulates its own expression in a feed forward loop via the regulatory protein Lrp. In conclusion, we have discovered novel antisense RNAs, e.g. miRNAs in D. discoideum, developed an approach to identify targets for antisense RNAs, i.e. a target prediction program for sRNAs in bacteria, and verified and characterized some of the predicted antisense RNA interactions.

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Chadwick, D. R. "Studies on antisense RNA inhibition of HIV-1 replication". Thesis, University of Cambridge, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.597386.

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Two vector systems were developed expressing antisense RNA (of two different sizes) complementary to three target regions in the 5' leader/LTR of HIV-1: the R (TAR) region, the primer binding site and the splice donor-packaging signal (ψ) region. After cloning these regions into an expression vector, pcDNA3, designed to express these sequences at high levels from the CMV IE promoter, stable constitutive expression in a T cell line was demonstrated by RT-PCR. After directly challenging these cell lines with HIV-1 at various doses cell lines expressing antisense RNA targeting the ψ-region showed significant inhibition of replication compared to cell lines expressing the same sequence in sense. A second, co-transfection assay using COS-1 cells was also developed to assess the antiviral capabilities of these vectors. Both sequences targeting the ψ-region and one sequence complementary to the TAR region inhibited expression of viral protein; furthermore analyses of relative levels of cellular and viral RNA from these assays suggested that each of these antisense molecules was exerting its effect at an early stage in the transcription-translation pathway. CXCR4, an important co-receptor for HIV was also targeted for down regulation by antisense RNA. Inducible expression of a sequence complementary to a region of this gene using the 'tet-on' system was accomplished leading to down-regulation of surface CXCR4 expression in T cells. Down-regulation appeared to result in reduced replication of HIV-1 in these cells. Genetic strategies for inhibiting HIV replication may provide an alternative and complementary approach to chemotherapy for infected individuals.

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Engdahl, Hilde Merete. "Natural and artificial antisense RNA : a study of inhibition of gene expression /". Uppsala : Swedish Univ. of Agricultural Sciences (Sveriges lantbruksuniv.), 2000. http://epsilon.slu.se/avh/2000/91-576-5784-X.pdf.

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Dong, Shuzhi Dong Shuzhi. "I. Restriction of DNA conformation by spirocyclic annulation at C-4' II. Studies toward the enantioselective synthesis of pestalotiopsin A /". Columbus, Ohio : Ohio State University, 2007. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1174627553.

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Libros sobre el tema "Antisense RNA"

A, Melton Douglas y Cold Spring Harbor Laboratory, eds. Antisense RNA and DNA. Cold Spring Harbor, N.Y: Cold Spring Harbor Laboratory, 1988.

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H, Murray James A., ed. Antisense RNA and DNA. New York: Wiley-Liss, 1992.

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1922-, Weiss Benjamin, ed. Antisense oligodeoxynucleotides and antisense RNA: Novel pharmacological and therapeutic agents. Roca Raton, Fla: CRC Press, 1997.

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1947-, Brakel Christine L., ed. Discoveries in antisense nucleic acids. The Woodlands, Tex: Portfolio Pub. Co., 1989.

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Arechavala-Gomeza, Virginia y Alejandro Garanto, eds. Antisense RNA Design, Delivery, and Analysis. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2010-6.

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Ian, Phillips M., ed. Antisense technology: General methods, methods of delivery and RNA studies. San Diego, CA: Academic Press, 1999.

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Ian, Phillips M., ed. Antisense technology: General methods, methods of delivery and RNA studies. San Diego, CA: Academic Press, 2000.

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Portmann, Stefan. Kristallstrukturanalysen von RNA-Sekundärstrukturelementen und Antisense-Oligonukleotiden. [s.l.]: [s.n.], 1996.

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1966-, Hartmann Gunther y Endres Stefan 1957-, eds. Manual of antisense methodology. Boston: Klwuer Academic, 1999.

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Ian, Phillips M., ed. Antisense technology: Applications. San Diego, CA: Academic Press, 2000.

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Capítulos de libros sobre el tema "Antisense RNA"

Scherrmann, Jean-Michel, Kim Wolff, Christine A. Franco, Marc N. Potenza, Tayfun Uzbay, Lisiane Bizarro, David C. S. Roberts et al. "Antisense RNA". En Encyclopedia of Psychopharmacology, 127. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-68706-1_1062.

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Nordström, Kurt, Stanley N. Cohen y Robert W. Simons. "Antisense RNA". En Post-transcriptional Control of Gene Expression, 231–61. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-60929-9_20.

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Houba-Hérin, N. y M. Inouye. "Antisense RNA". En Nucleic Acids and Molecular Biology, 210–20. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-46596-3_13.

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Gooch, Jan W. "Antisense RNA". En Encyclopedic Dictionary of Polymers, 875. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-6247-8_13155.

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Zeiler, Brian N. y Robert W. Simons. "Control by Antisense RNA". En Regulation of Gene Expression in Escherichia coli, 67–83. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4684-8601-8_5.

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Alkan, Can, Emre Karakoç, Joseph H. Nadeau, S. Cenk Şahinalp y Kaizhong Zhang. "RNA-RNA Interaction Prediction and Antisense RNA Target Search". En Lecture Notes in Computer Science, 152–71. Berlin, Heidelberg: Springer Berlin Heidelberg, 2005. http://dx.doi.org/10.1007/11415770_12.

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Harada, Kazuo. "Identification of Antisense RNA Stem-Loops That Inhibit RNA–Protein Interactions Using a Bacterial Reporter System". En RNA-RNA Interactions, 49–56. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1896-6_4.

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Georg, Jens y Wolfgang R. Hess. "Widespread Antisense Transcription in Prokaryotes". En Regulating with RNA in Bacteria and Archaea, 191–210. Washington, DC, USA: ASM Press, 2018. http://dx.doi.org/10.1128/9781683670247.ch12.

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Wong, Dominic W. S. "Improving Tomato Quality by Antisense RNA". En The ABCs of Gene Cloning, 143–47. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-77982-9_13.

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Yang, Yaping, Jian Wang, Ruihua Zhang y Yajun Yan. "Antisense RNA Elements for Downregulating Expression". En Methods in Molecular Biology, 23–35. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9142-6_3.

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Actas de conferencias sobre el tema "Antisense RNA"

Huang, Xin y Huang Huang. "Abstract 2434: Regulation of HIF1a stability by an antisense RNA". En Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-2434.

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Marzenell, Paul D., Helen Hagen, Larisa Kovbasyuk y Andriy Mokhir. "Chemically modified phosphorothioate DNA and 2'-OMe RNA as antisense agents". En XVth Symposium on Chemistry of Nucleic Acid Components. Prague: Institute of Organic Chemistry and Biochemistry, Academy of Sciences of the Czech Republic, 2011. http://dx.doi.org/10.1135/css201112391.

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Goodarzi, Hani, Bruce Culbertson, Kristle Garcia y Lisa Fish. "Abstract PS19-01: A sense-antisense RNA interaction drives metabolic reprogramming in metastatic breast cancer". En Abstracts: 2020 San Antonio Breast Cancer Virtual Symposium; December 8-11, 2020; San Antonio, Texas. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.sabcs20-ps19-01.

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Park, Jeong Eun, Lee Spraggon y Luca Cartegni. "Abstract LB-239: Induction of therapeutic soluble decoy EGFR variants by antisense manipulation of RNA processing". En Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-lb-239.

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Stewart, Greg L., Katey SS Enfield, David A. Rowbotham, Roland Hubaux, Victor Martinez, Stephen Lam y Wan Lam. "Abstract B26: OIP5-Antisense 1, a long noncoding RNA deregulated in non-small cell lung cancer". En Abstracts: AACR Special Conference on Noncoding RNAs and Cancer: Mechanisms to Medicines; December 4-7, 2015; Boston, MA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.nonrna15-b26.

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Vidarsdottir, Linda, Alireza Azimi, Jason Serviss, Christian Ingvar, Göran Jönsson, Håkan Olsson, Marianne Frostvik Stolt et al. "Abstract B28: PTENpg1 antisense RNA mediates PTEN suppression in vemurafenib resistance and predicts clinical outcome in melanoma patients". En Abstracts: AACR Special Conference on Noncoding RNAs and Cancer: Mechanisms to Medicines; December 4-7, 2015; Boston, MA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.nonrna15-b28.

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Hsu, Jeff, Guobin He, Gourab Bhattacharjee, Tianyuan Zhou, Chris May, Brett P. Monia, Youngsoo Kim y A. Robert MacLeod. "Abstract 2951: Potent antisense pharmacology of highly optimized antisense oligonucleotides in multiple transgenic, spontaneous and patient derived xenograft models of cancer reveals antitumor activity for the non-coding RNA MALAT-1." En Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-2951.

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Devadoss, D., G. Daly, M. Manevski, D. Houserova, S. S. Hussain, N. B. Schmid, M. A. Salathe, G. M. Borchert, R. J. Langley y H. S. Chand. "A Long Noncoding RNA Antisense to ICAM-1 Is Involved in Allergic Asthma Associated Hyperreactive Mucous Response of Airway Epithelial Cells". En American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a7398.

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Cartegni, Luca y lee Spraggon. "Abstract LB-318: Reshaping the cancer proteome: therapeutic targeting of signaling and resistance in cancer by antisense manipulation of RNA processing." En Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-lb-318.

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Akhmetova, E. A., O. V. Sergeeva y T. S. Zatsepin. "N-ALKYLSULFONYL MODIFICATIONS ARE PERSPECTIVE ANALOGOUS OF PHOSPHOROTHIOATES IN ANTISENSE OLIGONUCLEOTIDES AND GUIDE RNAS". En X Международная конференция молодых ученых: биоинформатиков, биотехнологов, биофизиков, вирусологов и молекулярных биологов — 2023. Novosibirsk State University, 2023. http://dx.doi.org/10.25205/978-5-4437-1526-1-271.

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The main disadvantages of therapeutic oligonucleotides are the off-target activity and poor stability in vivo. Major solutions of such limitations are chemical modification and targeted drug delivery. In current research we investigated the influence of alkylsulfonyl modifications on the efficacy of antisense oligonucleotides and gRNAs for CRISPR/Cas system in combination with different approaches of the selectivity improvement.

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Informes sobre el tema "Antisense RNA"

Chakraborty, Srijani. The Dawn of RNA Therapeutics. Spring Library, diciembre de 2020. http://dx.doi.org/10.47496/sl.blog.19.

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Williams, Briana J. The Effect of eIF4E Antisense RNA Expression on Prostate Tumor Angiogenesis and Growth. Fort Belvoir, VA: Defense Technical Information Center, septiembre de 1999. http://dx.doi.org/10.21236/ada383175.

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Cowell, John K. Targeted Therapy of Human Breast Cancer by 2-5A-Antisense Directed Against Telomerase RNA. Fort Belvoir, VA: Defense Technical Information Center, septiembre de 2002. http://dx.doi.org/10.21236/ada413348.

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Cowell, John K. Targeted Therapy of Human Breast Cancer by 2-5A-Antisense Directed Against Telomerase RNA. Fort Belvoir, VA: Defense Technical Information Center, diciembre de 2003. http://dx.doi.org/10.21236/ada424078.

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Liao, Jianhua, Jingting Liu, Baoqing Liu, Chunyan Meng y Peiwen Yuan. Effect of OIP5-AS1 on clinicopathological characteristics and prognosis of cancer patients: a meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, octubre de 2022. http://dx.doi.org/10.37766/inplasy2022.10.0118.

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Review question / Objective: According to recent studies, long non-coding RNA (lncRNAs) i.e., OPA-interacting protein 5 antisense RNA 1 (OIP5-AS1) has an important role in various carcinomas. However, its role in the cancer is contradictory. Therefore, we aimed to evaluate the link between OIP5-AS1 and cancer patients' clinicopathological characteristics and prognosis to better understand OIP5-AS1's role in cancer. Condition being studied: Reported studies have revealed that long non-coding RNA (lncRNAs) are considerably involved in crucial physiological events in several carcinomas, it can inhibit or promote the occurrence and development of tumors by changing the sequence and spatial structure, modulating epigenetic, regulating the expression level and interacting with binding proteins. However, the mechanism of cancer regulation via lncRNAs was incompletely understood. Hence, clarifying the application value of lncRNAs in preclinical and clinical disease diagnosis and treatment was therefore the prime objective in the field of cancer research at the time.

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Schuster, Gadi y David Stern. Integrated Studies of Chloroplast Ribonucleases. United States Department of Agriculture, septiembre de 2011. http://dx.doi.org/10.32747/2011.7697125.bard.

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Gene regulation at the RNA level encompasses multiple mechanisms in prokaryotes and eukaryotes, including splicing, editing, endo- and exonucleolytic cleavage, and various phenomena related to small or interfering RNAs. Ribonucleases are key players in nearly all of these post-transcriptional mechanisms, as the catalytic agents. This proposal continued BARD-funded research into ribonuclease activities in the chloroplast, where RNase mutation or deficiency can cause metabolic defects and is often associated with plant chlorosis, embryo or seedling lethality, and/or failure to tolerate nutrient stress. The first objective of this proposal was to examined a series of point mutations in the PNPase enzyme of Arabidopsis both in vivo and in vitro. This goal is related to structure-function analysis of an enzyme whose importance in many cellular processes in prokaryotes and eukaryotes has only begun to be uncovered. PNPase substrates are mostly generated by endonucleolytic cleavages for which the catalytic enzymes remain poorly described. The second objective of the proposal was to examine two candidate enzymes, RNase E and RNase J. RNase E is well-described in bacteria but its function in plants was still unknown. We hypothesized it catalyzes endonucleolytic cleavages in both RNA maturation and decay. RNase J was recently discovered in bacteria but like RNase E, its function in plants had yet to be explored. The results of this work are described in the scientific manuscripts attached to this report. We have completed the first objective of characterizing in detail TILLING mutants of PNPase Arabidopsis plants and in parallel introducing the same amino acids changes in the protein and characterize the properties of the modified proteins in vitro. This study defined the roles for both RNase PH core domains in polyadenylation, RNA 3’-end maturation and intron degradation. The results are described in the collaborative scientific manuscript (Germain et al 2011). The second part of the project aimed at the characterization of the two endoribonucleases, RNase E and RNase J, also in this case, in vivo and in vitro. Our results described the limited role of RNase E as compared to the pronounced one of RNase J in the elimination of antisense transcripts in the chloroplast (Schein et al 2008; Sharwood et al 2011). In addition, we characterized polyadenylation in the chloroplast of the green alga Chlamydomonas reinhardtii, and in Arabidopsis (Zimmer et al 2009). Our long term collaboration enabling in vivo and in vitro analysis, capturing the expertise of the two collaborating laboratories, has resulted in a biologically significant correlation of biochemical and in planta results for conserved and indispensable ribonucleases. These new insights into chloroplast gene regulation will ultimately support plant improvement for agriculture.

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Levy, Avraham A. y Virginia Walbot. Regulation of Transposable Element Activities during Plant Development. United States Department of Agriculture, agosto de 1992. http://dx.doi.org/10.32747/1992.7568091.bard.

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We have studied the regulation of the maize Ac and MuDR transposable elements activities during plant development. Ac was studied in an heterologous system (transgenic tobacco plants and cell suspensions) while MuDR was studied in the native maize background. The focus of this study was on the transcriptional regulation of Ac and MuDR. For Ac, the major achievements were to show that 1-It is autoregulated in a way that the Ac-encoded transposase can repress the activity of its own promoter; 2-It is expressed at low basal level in all the plant organs that were studied, and its activity is stronger in dividing tissues -- a behaviour reminiscent of housekeeping genes; 3- the activity of Ac promoter is cell cycle regulated -- induced at early S-phase and increasing until mitosis; 4- host factor binding sites were identified at both extremities of Ac and may be important for transposition. For MuDR, It was shown that it encodes two genes, mudrA and mudrB, convergently transcribed from near-identical promoters in the terminal inverted repeats. Distinct 5' start sites, alternative splicing, production of antisense RNA and tissue specificity were all shown to be involved in the regulation of MuDR.

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Flaishman, Moshe, Herb Aldwinckle, Shulamit Manulis y Mickael Malnoy. Efficient screening of antibacterial genes by juvenile phase free technology for developing resistance to fire blight in pear and apple trees. United States Department of Agriculture, diciembre de 2008. http://dx.doi.org/10.32747/2008.7613881.bard.

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Objectives: The original objectives of this project were to: Produce juvenile-free pear and apple plants and examine their sensitivity to E. amylovora; Design novel vectors, for antibacterial proteins and promoters expression, combined with the antisense TFL1 gene, and transformation of Spadona pear in Israel and Galaxy apple in USA. The original objectives were revised from the development of novel vectors with antibacterial proteins combined with the TFL-1 due to the inefficiency of alternative markes initially evaluated in pear, phoshomannose-isomerase and 2-deoxyglucose-6-phosphate phosphatase and the lack of development of double selection system. The objectives of project were revised to focus primarily on the development additional juvenile free systems by the use of another pear variety and manipulation of the FT gene under the control of several promoters. Based on the results creation of fire blight resistance pear variety was developed by the use of the juvenile free transgenic plant. Background: Young tree seedlings are unable to initiate reproductive organs and require a long period of shoot maturation, known as juvenile phase. In pear, juvenile period can last 5-7 years and it causes a major delay in breeding programs. We isolated the TFL1 gene from Spadona pear (PcTFL1-1) and produced transgenic ‘Spadona’ trees silencing the PcTFL1 gene using a RNAi approach. Transgenic tissue culture ‘Spadona’ pear flowered in vitro. As expected, the expression of the endogenous PcTFL1 was suppressed in the transgenic line that showed precocious flowering. Transgenic plants were successfully rooted in the greenhouse and most of the plants flowered after only 4-8 months, whereas the non-transformed control plants have flowered only after 5-6 years of development. Major achievements: Prior to flower induction, transgenic TFL1-RNAi ‘Spadona’ plants developed a few branches and leaves. Flower production in the small trees suppressed the development of the vegetative branches, thus resulting in compact flowering trees. Flowering was initiated in terminal buds, as described for the Arabidopsis tfl1 mutant. Propagation of the transgenic TFL1-RNAi ‘Spadona’ was performed by bud grafting on 'Betulifolia' rootstock and resulted in compact flowering trees. The transgenic flowering grafted plants were grown in the greenhouse under a long photoperiod for one year, and flowered continuously. Pollination of the transgenic flowers with ‘Costia‘ pear pollen generated fruits of regular shape with fertile F1 seeds. The F1 transgenic seedling grown in the greenhouse formed shoots and produced terminal flowers only five months after germination. In addition, grafted F1 transgenic buds flower and fruit continuously, generating hybrid fruits with regular shape, color and taste. Several pear varieties were pollinated with the transgenic TFL1-RNAi ‘Spadona’ pollen including `Herald Harw` that was reported to have resistance to fire blight diseases. The F-1 hybrid seedlings currently grow in our greenhouse. We conclude that the juvenile-free transgenic ‘Spadona’ pear enables the development of a fast breeding method in pear that will enable us to generate a resistance pear to fire blight. Implications: The research supported by this grant has demonstrated the use of transgenic juvenile free technology in pear. The use of the juvenile free technology for enhancement of conventional breeding in fruit tree will serve to enhance fast breeding systems in pear and another fruit trees.

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Granot, David y Noel Michelle Holbrook. Role of Fructokinases in the Development and Function of the Vascular System. United States Department of Agriculture, enero de 2011. http://dx.doi.org/10.32747/2011.7592125.bard.

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Plant vascular tissues are superhighways whose development and function have profound implications for productivity, yield and stress response. Preliminary studies by the PI indicated that sugar metabolism mediated by fructokinases (FRKs) has a pronounced effect on the transport properties of the xylem. The goal of this research was to determine how the main fructokinase gene, FRK2, and the only plastidic fructokinase, FRK3, influence vascular development and physiology, emphasizing processes that occur at both the cellular and organismic level. We found that both genes are expressed in vascular tissues, but FRK3 is expressed primarily in vascular tissues of mature petioles. Vascular anatomy of plants with antisense suppression of FRK2 uncovered that FRK2 is necessary for xylem and phloem development, most likely due to its role in vascular cell-wall synthesis, and affects vascular development all over the plant. As a result, suppression of FRK2 reduced hydraulic conductivity of roots, stem and leaves and restricted sugar phloem transport. Vascular anatomy of plants with RNAi suppression of FRK3 uncovered that FRK3 is required for vascular development in mature petiole but its role is partially complemented by FRK2. Suppression of FRK3 combined with partial suppression of FRK2 had effects completely different from that of FRK2 suppression, resulting in wilting of mature leaves rather than young leaves of FRK2 suppressed plants, and decreased export of photoassimilates. This primary effect of FRK2 suppression on mature petioles had a secondary effect, reducing the hydraulic conductivity in roots and stem. The very fact that a plastidic fructokinase plays a role in vascular development is quite surprising and we are still seeking to uncover its metabolic mode-of-action. Yet, it is clear that these two fructokinases have different roles in the coordination between photosynthetic capacity and vascular development. We have started analyzing the role of the last third FRK, FRK1, and discovered that it is also expressed exclusively in vascular tissues. It appears therefore, that all FRKs studied here are involved in vascular development. An interesting unexpected outcome of this study was the connection of FRK2 with hormonal regulation of vascular development, most likely auxin. This observation together with the yet to be solved questions on the exact roles of FRK3 are the subjects of our current efforts.

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