Relevant bibliographies by topics / -1 ribosomal frameshifting

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Academic literature on the topic '-1 ribosomal frameshifting'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "-1 ribosomal frameshifting"

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Lopinski, John D., Jonathan D. Dinman, and Jeremy A. Bruenn. "Kinetics of Ribosomal Pausing during Programmed −1 Translational Frameshifting." Molecular and Cellular Biology 20, no. 4 (February 15, 2000): 1095–103. http://dx.doi.org/10.1128/mcb.20.4.1095-1103.2000.

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ABSTRACT In the Saccharomyces cerevisiae double-stranded RNA virus, programmed −1 ribosomal frameshifting is responsible for translation of the second open reading frame of the essential viral RNA. A typical slippery site and downstream pseudoknot are necessary for this frameshifting event, and previous work has demonstrated that ribosomes pause over the slippery site. The translational intermediate associated with a ribosome paused at this position is detected, and, using in vitro translation and quantitative heelprinting, the rates of synthesis, the ribosomal pause time, the proportion of ribosomes paused at the slippery site, and the fraction of paused ribosomes that frameshift are estimated. About 10% of ribosomes pause at the slippery site in vitro, and some 60% of these continue in the −1 frame. Ribosomes that continue in the −1 frame pause about 10 times longer than it takes to complete a peptide bond in vitro. Altering the rate of translational initiation alters the rate of frameshifting in vivo. Our in vitro and in vivo experiments can best be interpreted to mean that there are three methods by which ribosomes pass the frameshift site, only one of which results in frameshifting.
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Choi, Junhong, Sinéad O’Loughlin, John F. Atkins, and Joseph D. Puglisi. "The energy landscape of −1 ribosomal frameshifting." Science Advances 6, no. 1 (January 2020): eaax6969. http://dx.doi.org/10.1126/sciadv.aax6969.

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Maintenance of translational reading frame ensures the fidelity of information transfer during protein synthesis. Yet, programmed ribosomal frameshifting sequences within the coding region promote a high rate of reading frame change at predetermined sites thus enriching genomic information density. Frameshifting is typically stimulated by the presence of 3′ messenger RNA (mRNA) structures, but how these mRNA structures enhance −1 frameshifting remains debatable. Here, we apply single-molecule and ensemble approaches to formulate a mechanistic model of ribosomal −1 frameshifting. Our model suggests that the ribosome is intrinsically susceptible to frameshift before its translocation and this transient state is prolonged by the presence of a precisely positioned downstream mRNA structure. We challenged this model using temperature variation in vivo, which followed the prediction made based on in vitro results. Our results provide a quantitative framework for analyzing other frameshifting enhancers and a potential approach to control gene expression dynamically using programmed frameshifting.
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Huang, Wan-Ping, Che-Pei Cho, and Kung-Yao Chang. "mRNA-Mediated Duplexes Play Dual Roles in the Regulation of Bidirectional Ribosomal Frameshifting." International Journal of Molecular Sciences 19, no. 12 (December 4, 2018): 3867. http://dx.doi.org/10.3390/ijms19123867.

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In contrast to −1 programmed ribosomal frameshifting (PRF) stimulation by an RNA pseudoknot downstream of frameshifting sites, a refolding upstream RNA hairpin juxtaposing the frameshifting sites attenuates −1 PRF in human cells and stimulates +1 frameshifting in yeast. This eukaryotic functional mimicry of the internal Shine-Dalgarno (SD) sequence-mediated duplex was confirmed directly in the 70S translation system, indicating that both frameshifting regulation activities of upstream hairpin are conserved between 70S and 80S ribosomes. Unexpectedly, a downstream pseudoknot also possessed two opposing hungry codon-mediated frameshifting regulation activities: attenuation of +1 frameshifting and stimulation of a non-canonical −1 frameshifting within the +1 frameshift-prone CUUUGA frameshifting site in the absence of release factor 2 (RF2) in vitro. However, the −1 frameshifting activity of the downstream pseudoknot is not coupled with its +1 frameshifting attenuation ability. Similarly, the +1 frameshifting activity of the upstream hairpin is not required for its −1 frameshifting attenuation function Thus, each of the mRNA duplexes flanking the two ends of a ribosomal mRNA-binding channel possesses two functions in bi-directional ribosomal frameshifting regulation: frameshifting stimulation and counteracting the frameshifting activity of each other.
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Kontos, Harry, Sawsan Napthine, and Ian Brierley. "Ribosomal Pausing at a Frameshifter RNA Pseudoknot Is Sensitive to Reading Phase but Shows Little Correlation with Frameshift Efficiency." Molecular and Cellular Biology 21, no. 24 (December 15, 2001): 8657–70. http://dx.doi.org/10.1128/mcb.21.24.8657-8670.2001.

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ABSTRACT Here we investigated ribosomal pausing at sites of programmed −1 ribosomal frameshifting, using translational elongation and ribosome heelprint assays. The site of pausing at the frameshift signal of infectious bronchitis virus (IBV) was determined and was consistent with an RNA pseudoknot-induced pause that placed the ribosomal P- and A-sites over the slippery sequence. Similarly, pausing at the simian retrovirus 1 gag/pol signal, which contains a different kind of frameshifter pseudoknot, also placed the ribosome over the slippery sequence, supporting a role for pausing in frameshifting. However, a simple correlation between pausing and frameshifting was lacking. Firstly, a stem-loop structure closely related to the IBV pseudoknot, although unable to stimulate efficient frameshifting, paused ribosomes to a similar extent and at the same place on the mRNA as a parental pseudoknot. Secondly, an identical pausing pattern was induced by two pseudoknots differing only by a single loop 2 nucleotide yet with different functionalities in frameshifting. The final observation arose from an assessment of the impact of reading phase on pausing. Given that ribosomes advance in triplet fashion, we tested whether the reading frame in which ribosomes encounter an RNA structure (the reading phase) would influence pausing. We found that the reading phase did influence pausing but unexpectedly, the mRNA with the pseudoknot in the phase which gave the least pausing was found to promote frameshifting more efficiently than the other variants. Overall, these experiments support the view that pausing alone is insufficient to mediate frameshifting and additional events are required. The phase dependence of pausing may be indicative of an activity in the ribosome that requires an optimal contact with mRNA secondary structures for efficient unwinding.
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Meskauskas, Arturas, Jennifer L. Baxter, Edward A. Carr, Jason Yasenchak, Jennifer E. G. Gallagher, Susan J. Baserga, and Jonathan D. Dinman. "Delayed rRNA Processing Results in Significant Ribosome Biogenesis and Functional Defects." Molecular and Cellular Biology 23, no. 5 (March 1, 2003): 1602–13. http://dx.doi.org/10.1128/mcb.23.5.1602-1613.2003.

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ABSTRACT mof6-1 was originally isolated as a recessive mutation in Saccharomyces cerevisiae which promoted increased efficiencies of programmed −1 ribosomal frameshifting and rendered cells unable to maintain the killer virus. Here, we demonstrate that mof6-1 is a unique allele of the histone deacetylase RPD3, that the deacetylase function of Rpd3p is required for controlling wild-type levels of frameshifting and virus maintenance, and that the closest human homolog can fully complement these defects. Loss of the Rpd3p-associated histone deacetylase function, either by mutants of rpd3 or loss of the associated gene product Sin3p or Sap30p, results in a delay in rRNA processing rather than in an rRNA transcriptional defect. This results in production of ribosomes having lower affinities for aminoacyl-tRNA and diminished peptidyltransferase activities. We hypothesize that decreased rates of peptidyl transfer allow ribosomes with both A and P sites occupied by tRNAs to pause for longer periods of time at −1 frameshift signals, promoting increased programmed −1 ribosomal frameshifting efficiencies and subsequent loss of the killer virus. The frameshifting defect is accentuated when the demand for ribosomes is highest, suggesting that rRNA posttranscriptional modification is the bottleneck in ribosome biogenesis.
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Finch, Leanne K., Roger Ling, Sawsan Napthine, Allan Olspert, Thomas Michiels, Cécile Lardinois, Susanne Bell, Gary Loughran, Ian Brierley, and Andrew E. Firth. "Characterization of Ribosomal Frameshifting in Theiler's Murine Encephalomyelitis Virus." Journal of Virology 89, no. 16 (June 10, 2015): 8580–89. http://dx.doi.org/10.1128/jvi.01043-15.

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ABSTRACTTheiler's murine encephalomyelitis virus(TMEV) is a member of the genusCardiovirusin thePicornaviridae, a family of positive-sense single-stranded RNA viruses. Previously, we demonstrated that in the related cardiovirus,Encephalomyocarditis virus, a programmed −1 ribosomal frameshift (−1 PRF) occurs at a conserved G_GUU_UUU sequence within the 2B-encoding region of the polyprotein open reading frame (ORF). Here we show that −1 PRF occurs at a similar site during translation of the TMEV genome. In addition, we demonstrate that a predicted 3′ RNA stem-loop structure at a noncanonical spacing downstream of the shift site is required for efficient frameshifting in TMEV and that frameshifting also requires virus infection. Mutating the G_GUU_UUU shift site to inhibit frameshifting results in an attenuated virus with reduced growth kinetics and a small-plaque phenotype. Frameshifting in the virus context was found to be extremely efficient at 74 to 82%, which, to our knowledge, is the highest frameshifting efficiency recorded to date for any virus. We propose that highly efficient −1 PRF in TMEV provides a mechanism to escape the confines of equimolar expression normally inherent in the single-polyprotein expression strategy of picornaviruses.IMPORTANCEMany viruses utilize programmed −1 ribosomal frameshifting (−1 PRF) to produce different protein products at a defined ratio, or to translate overlapping ORFs to increase coding capacity. With few exceptions, −1 PRF occurs on specific “slippery” heptanucleotide sequences and is stimulated by RNA structure beginning 5 to 9 nucleotides (nt) downstream of the slippery site. Here we describe an unusual case of −1 PRF in Theiler's murine encephalomyelitis virus (TMEV) that is extraordinarily efficient (74 to 82% of ribosomes shift into the alternative reading frame) and, in stark contrast to other examples of −1 PRF, is dependent upon a stem-loop structure beginning 14 nt downstream of the slippery site. Furthermore, in TMEV-based reporter constructs in transfected cells, efficient frameshifting is critically dependent upon virus infection. We suggest that TMEV evolved frameshifting as a novel mechanism for removing ribosomes from the message (a “ribosome sink”) to downregulate synthesis of the 3′-encoded replication proteins.
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Xie, Ping. "Dynamics of +1 ribosomal frameshifting." Mathematical Biosciences 249 (March 2014): 44–51. http://dx.doi.org/10.1016/j.mbs.2014.01.008.

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Ramos, F. Dos, M. Carrasco, T. Doyle, and I. Brierley. "Programmed −1 ribosomal frameshifting in the SARS coronavirus." Biochemical Society Transactions 32, no. 6 (October 26, 2004): 1081–83. http://dx.doi.org/10.1042/bst0321081.

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Programmed −1 ribosomal frameshifting is an alternate mechanism of translation used by coronavirus to synthesize replication proteins encoded by two overlapping open reading frames. For some coronaviruses, the mRNA cis-acting stimulatory structures involved in this process have been characterized, but their precise contribution to ribosomal frameshifting is not completely understood. Recently, a novel coronavirus was identified as the causative agent of the severe acute respiratory syndrome. This review describes the mRNA motifs involved in programmed −1 ribosomal frameshifting in this virus.
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Cao, Song, and Shi-Jie Chen. "Predicting ribosomal frameshifting efficiency." Physical Biology 5, no. 1 (March 11, 2008): 016002. http://dx.doi.org/10.1088/1478-3975/5/1/016002.

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Tumer, Nilgun E., Bijal A. Parikh, Ping Li, and Jonathan D. Dinman. "The Pokeweed Antiviral Protein Specifically Inhibits Ty1-Directed +1 Ribosomal Frameshifting and Retrotransposition in Saccharomyces cerevisiae." Journal of Virology 72, no. 2 (February 1, 1998): 1036–42. http://dx.doi.org/10.1128/jvi.72.2.1036-1042.1998.

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ABSTRACT Programmed ribosomal frameshifting is a molecular mechanism that is used by many RNA viruses to produce Gag-Pol fusion proteins. The efficiency of these frameshift events determines the ratio of viral Gag to Gag-Pol proteins available for viral particle morphogenesis, and changes in ribosomal frameshift efficiencies can severely inhibit virus propagation. Since ribosomal frameshifting occurs during the elongation phase of protein translation, it is reasonable to hypothesize that agents that affect the different steps in this process may also have an impact on programmed ribosomal frameshifting. We examined the molecular mechanisms governing programmed ribosomal frameshifting by using two viruses of the yeast Saccharomyces cerevisiae. Here, we present evidence that pokeweed antiviral protein (PAP), a single-chain ribosomal inhibitory protein that depurinates an adenine residue in the α-sarcin loop of 25S rRNA and inhibits translocation, specifically inhibits Ty1-directed +1 ribosomal frameshifting in intact yeast cells and in an in vitro assay system. Using an in vivo assay for Ty1 retrotransposition, we show that PAP specifically inhibits Ty1 retrotransposition, suggesting that Ty1 viral particle morphogenesis is inhibited in infected cells. PAP does not affect programmed −1 ribosomal frameshift efficiencies, nor does it have a noticeable impact on the ability of cells to maintain the M1-dependent killer virus phenotype, suggesting that −1 ribosomal frameshifting does not occur after the peptidyltransferase reaction. These results provide the first evidence that PAP has viral RNA-specific effects in vivo which may be responsible for the mechanism of its antiviral activity.
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Dissertations / Theses on the topic "-1 ribosomal frameshifting"

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Bailey, Brenae L. "Stochastic Models of –1 Programmed Ribosomal Frameshifting." Diss., The University of Arizona, 2014. http://hdl.handle.net/10150/320007.

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Many viruses can produce multiple proteins from a single mRNA sequence by encoding the proteins in overlapping genes. One mechanism that causes the ribosomes of infected cells to decode both genes is –1 programmed ribosomal frameshifting. In this process, structural elements of the viral mRNA signal the ribosome to shift reading frames at a specific point. Although –1 frameshifting has been recognized since 1985, the mechanism is not well understood. I have developed a stochastic model of mRNA translation that includes the possibility of a –1 frameshift at any codon. The transition probabilities between states of the model are based on the energetics of local molecular interactions. The model reproduces observed translation rates as well as both the location and efficiency of frameshift events in the HIV-1 gag-pol sequence. In this work, the model is used to predict changes in the frameshift efficiency due to mutations in the viral mRNA sequence or variations in relative tRNA abundances. The model is sensitive to the size of the translating ribosome and to assumptions about the unfolding pathway of the stimulatory structure. As knowledge in the field of RNA structure prediction grows, that knowledge can be incorporated into the model developed here to make improved predictions. The single-ribosome translation model has been extended to polysomes by including initiation and termination rates and an exclusion principle, and allowing the stimulatory structure to refold on an appropriate timescale. The predicted frameshift efficiency for a given mRNA can be tuned by varying the ribosome density on the mRNA. This finding affects the interpretation of frameshift efficiencies measured in the lab. In the parameter regime where translation is initiation-limited, the frameshift efficiency also depends on the structure refolding rate, which determines the availability of the downstream structure for stimulating –1 frameshifts. Furthermore, there is a trade-off between frameshift efficiency and protein synthesis rate.
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Vidaković, Marijana. "Studies of -1 ribosomal frameshifting in virus systems." Thesis, University of Cambridge, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.621823.

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Neeriemer, Jessica Joy. "Programmed ribosomal frameshifting in SARS-CoV and HIV-1." College Park, Md.: University of Maryland, 2007. http://hdl.handle.net/1903/7713.

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Thesis (M.S.) -- University of Maryland, College Park, 2007.
Thesis research directed by: Dept. of Cell Biology & Molecular Genetics. 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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Nikolić, Emily Isabel Cinzia. "Structural and functional studies of programmed -1 ribosomal frameshifting." Thesis, University of Cambridge, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.607928.

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King, Louise Margaret. "Studies of programmed -1 ribosomal frameshifting in virus systems." Thesis, University of Cambridge, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.615622.

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Kontos, Charalampos. "A molecular analysis of the role of ribosomal pausing in -1 ribosomal frameshifting." Thesis, University of Cambridge, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.624652.

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Ramarao, Rachana. "Molecular studies of programmed -1 ribosomal frameshifting and translational readthrough." Thesis, University of Cambridge, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.615726.

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Liphardt, Jan Tage Carl. "The mechanism of -1 ribosomal frameshifting : experimental and theoretical analysis." Thesis, University of Cambridge, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.621577.

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Pennell, Simon John. "Structural studies of RNA pseudoknots involved in programmed -1 ribosomal frameshifting." Thesis, University of Cambridge, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.620323.

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Wang, Guan. "STRUCTURAL STUDY OF HUMAN CATENIN ΒETA-LIKE PROTEIN 1 AND DOUBLE RNA PSEUDOKNOTS IN -1 RIBOSOMAL FRAMESHIFTING." OpenSIUC, 2015. https://opensiuc.lib.siu.edu/dissertations/993.

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Project 1-- structure determination of human catenin-β-like protein 1 by x-ray crystallography Catenin-β-like protein 1 (CTNNBL1) is a highly conserved protein with multiple functions, one of which is to act as an interaction partner of the antibody-diversification enzyme activation-induced cytidine deaminase (AID) for its nuclear import and subnuclear trafficking. In this dissertation, the crystal structure of full-length human CTNNBL1 is reported. The protein contains six armadillo (ARM) repeats that pack into a superhelical ARM domain. This ARM domain is unique within the ARM protein family owing to the presence of several unusual structural features. Moreover, CTNNBL1 contains significant and novel non-ARM structures flanking both ends of the central ARM domain. A strong continuous hydrophobic core runs through the whole structure, indicating that the ARM and non-ARM structures fold together to form an integral structure. This structure defines a highly restrictive and discriminatory protein-binding groove that is not observed in other ARM proteins. The presence of a cluster of histidine residues in the groove implies a pH-sensitive histidine-mediated mechanism that may regulate protein binding activity. The many unique structural features of CTNNBL1 establish it as a distinct member of the ARM protein family. The structure provides critical insights into the molecular interactions between CTNNBL1 and its protein partners, especially AID. Project 2 -- study of double pseudoknots in the regulation of -1 programmed ribosomal frameshifting in RNA viruses −1 programmed ribosomal frameshifting (PRF) is utilized by many viruses to synthesize their enzymatic and structural proteins at a defined ratio. For efficient −1 PRF, two cis-acting elements are required--a heptanucleotide frameshift site and a downstream stimulator such as a pseudoknot. By searching for all possible pseudoknots within the full-length viral genomic mRNAs, we detected potential double pseudoknots at the −1 PRF junction in several animal viruses, including human immunodeficiency virus type-1 (HIV-1), transmissible gastroenteritis virus (TGEV), Barmah Forest virus (BFV), Fort Morgan virus (FMV), and Equine arteritis virus (EAV). We built structural models of the HIV-1 and EAV double pseudoknots to show that both the tandem and embedded mode of double pseudoknots are feasible and reasonable. We hypothesize that the fundamental reason for the viruses to utilize coaxially stacked double pseudoknots is to increase the overall stability of the frameshift regulating structure and while avoiding the use of an ultra stable single pseudoknot which may become a ribosomal roadblock. Results from this study significantly expand the repertoire of RNA structures and dynamics that may involve in the regulation of −1 PRF in viruses
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Book chapters on the topic "-1 ribosomal frameshifting"

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Dinman, Jonathan D. "Programmed –1 Ribosomal Frameshifting in SARS Coronavirus." In Molecular Biology of the SARS-Coronavirus, 63–72. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-642-03683-5_5.

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Lewis, Terry L., and Suzanne M. Matsui. "Studies of the Astrovirus Signal That Induces (−1) Ribosomal Frameshifting." In Advances in Experimental Medicine and Biology, 323–30. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4899-1828-4_53.

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Brierley, Ian, Robert J. C. Gilbert, and Simon Pennell. "Pseudoknot-Dependent Programmed —1 Ribosomal Frameshifting: Structures, Mechanisms and Models." In Recoding: Expansion of Decoding Rules Enriches Gene Expression, 149–74. New York, NY: Springer New York, 2009. http://dx.doi.org/10.1007/978-0-387-89382-2_7.

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Fayet, Olivier, and Marie-Françoise Prère. "Programmed Ribosomal −1 Frameshifting as a Tradition: The Bacterial Transposable Elements of the IS3 Family." In Recoding: Expansion of Decoding Rules Enriches Gene Expression, 259–80. New York, NY: Springer New York, 2009. http://dx.doi.org/10.1007/978-0-387-89382-2_12.

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Atkins, J. F., K. Herbst, M. O’Connor, T. M. F. Tuohy, R. B. Weiss, N. M. Wills, and R. F. Gesteland. "Mutants of tRNA, Ribosomes and mRNA Affecting Frameshifting, Hopping or Stop Codon Read-Through." In The Translational Apparatus, 371–74. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-2407-6_35.

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Weiss, Robert B., Diane M. Dunn, John F. Atkins, and Raymond F. Gesteland. "Ribosomal Frameshifting from -2 to +50 Nucleotides." In Progress in Nucleic Acid Research and Molecular Biology, 159–83. Elsevier, 1990. http://dx.doi.org/10.1016/s0079-6603(08)60626-1.

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Visscher, Koen. "−1 Programmed Ribosomal Frameshifting as a Force-Dependent Process." In Progress in Molecular Biology and Translational Science, 45–72. Elsevier, 2016. http://dx.doi.org/10.1016/bs.pmbts.2015.11.003.

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"Drugs Targeting the -1 Ribosomal Frameshifting that Generates the Enzymes of the Human Immunodeficiency Virus." In Frontiers in Clinical Drug Research: HIV, edited by Léa Brakier-Gingras, Johanie Charbonneau, and Benjamin L. Miller, 67–82. BENTHAM SCIENCE PUBLISHERS, 2014. http://dx.doi.org/10.2174/9781608058969114010005.

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Conference papers on the topic "-1 ribosomal frameshifting"

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Khan, Yousuf A., Sergey O. Sulima, Joe Kendra, Vivek M. Advani, John E. Jones, Joseph Briggs, Kim de Keersmaecker, and Jonathan D. Dinman. "Abstract 3034: A programmed ribosomal frameshifting defect potentiates the transforming activity of the JAK2-V617F mutation." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-3034.

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