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Relevant bibliographies by topics / CUG

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Academic literature on the topic 'CUG'

Author: Grafiati

Published: 4 June 2021

Last updated: 17 February 2022

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Journal articles on the topic "CUG"

1

Tamjar, Jevgenia, Elizaveta Katorcha, Alexander Popov, and Lucy Malinina. "Structural dynamics of double-helical RNAs composed of CUG/CUG- and CUG/CGG-repeats." Journal of Biomolecular Structure and Dynamics 30, no. 5 (September 2012): 505–23. http://dx.doi.org/10.1080/07391102.2012.687517.

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Reddy, Kaalak, Jana R. Jenquin, Ona L. McConnell, John D. Cleary, Jared I. Richardson, Belinda S. Pinto, Maja C. Haerle, et al. "A CTG repeat-selective chemical screen identifies microtubule inhibitors as selective modulators of toxic CUG RNA levels." Proceedings of the National Academy of Sciences 116, no. 42 (September 30, 2019): 20991–1000. http://dx.doi.org/10.1073/pnas.1901893116.

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A CTG repeat expansion in the DMPK gene is the causative mutation of myotonic dystrophy type 1 (DM1). Transcription of the expanded CTG repeat produces toxic gain-of-function CUG RNA, leading to disease symptoms. A screening platform that targets production or stability of the toxic CUG RNA in a selective manner has the potential to provide new biological and therapeutic insights. A DM1 HeLa cell model was generated that stably expresses a toxic r(CUG)480 and an analogous r(CUG)0 control from DMPK and was used to measure the ratio-metric level of r(CUG)480 versus r(CUG)0. This DM1 HeLa model recapitulates pathogenic hallmarks of DM1, including CUG ribonuclear foci and missplicing of pre-mRNA targets of the muscleblind (MBNL) alternative splicing factors. Repeat-selective screening using this cell line led to the unexpected identification of multiple microtubule inhibitors as hits that selectively reduce r(CUG)480 levels and partially rescue MBNL-dependent missplicing. These results were validated by using the Food and Drug Administration-approved clinical microtubule inhibitor colchicine in DM1 mouse and primary patient cell models. The mechanism of action was found to involve selective reduced transcription of the CTG expansion that we hypothesize to involve the LINC (linker of nucleoskeleton and cytoskeleton) complex. The unanticipated identification of microtubule inhibitors as selective modulators of toxic CUG RNA opens research directions for this form of muscular dystrophy and may shed light on the biology of CTG repeat expansion and inform therapeutic avenues. This approach has the potential to identify modulators of expanded repeat-containing gene expression for over 30 microsatellite expansion disorders.

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Angelbello, Alicia J., Suzanne G. Rzuczek, Kendra K. Mckee, Jonathan L. Chen, Hailey Olafson, Michael D. Cameron, Walter N. Moss, Eric T. Wang, and Matthew D. Disney. "Precise small-molecule cleavage of an r(CUG) repeat expansion in a myotonic dystrophy mouse model." Proceedings of the National Academy of Sciences 116, no. 16 (March 29, 2019): 7799–804. http://dx.doi.org/10.1073/pnas.1901484116.

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Myotonic dystrophy type 1 (DM1) is an incurable neuromuscular disorder caused by an expanded CTG repeat that is transcribed into r(CUG)exp. The RNA repeat expansion sequesters regulatory proteins such as Muscleblind-like protein 1 (MBNL1), which causes pre-mRNA splicing defects. The disease-causing r(CUG)exp has been targeted by antisense oligonucleotides, CRISPR-based approaches, and RNA-targeting small molecules. Herein, we describe a designer small molecule, Cugamycin, that recognizes the structure of r(CUG)exp and cleaves it in both DM1 patient-derived myotubes and a DM1 mouse model, leaving short repeats of r(CUG) untouched. In contrast, oligonucleotides that recognize r(CUG) sequence rather than structure cleave both long and short r(CUG)-containing transcripts. Transcriptomic, histological, and phenotypic studies demonstrate that Cugamycin broadly and specifically relieves DM1-associated defects in vivo without detectable off-targets. Thus, small molecules that bind and cleave RNA have utility as lead chemical probes and medicines and can selectively target disease-causing RNA structures to broadly improve defects in preclinical animal models.

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Lee, Johanna E., and Thomas A. Cooper. "Pathogenic mechanisms of myotonic dystrophy." Biochemical Society Transactions 37, no. 6 (November 19, 2009): 1281–86. http://dx.doi.org/10.1042/bst0371281.

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DM (myotonic dystrophy) is a dominantly inherited genetic disorder that is the most common cause of muscular dystrophy in adults affecting 1 in 8500 individuals worldwide. Different microsatellite expansions in two loci cause different forms of the disease that share similar features: DM1 (DM type 1) is caused by a tri- (CTG) nucleotide expansion within the DMPK (dystrophia myotonica protein kinase) 3′-untranslated region and DM2 (DM type 2) is caused by a tetra- (CCTG) nucleotide expansion within intron 1 of the ZNF9 (zinc finger 9) gene. The pathogenic mechanism of this disease involves the RNA transcribed from the expanded allele containing long tracts of (CUG)n or (CCUG)n. The RNA results in a toxic effect through two RNA-binding proteins: MBNL1 (muscleblind-like 1) and CUGBP1 (CUG-binding protein 1). In DM1, MBNL1 is sequestered on CUG repeat-containing RNA resulting in its loss-of-function, while CUGBP1 is up-regulated through a signalling pathway. The downstream effects include disrupted regulation of alternative splicing, mRNA translation and mRNA stability, which contribute to the multiple features of DM1. This review will focus on the RNA gain-of-function disease mechanism, the important roles of MBNL1 and CUGBP1 in DM1, and the relevance to other RNA dominant disorders.

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Jasinska, Anna J., Piotr Kozlowski, and Wlodzimierz J. Krzyzosiak. "Expression characteristics of triplet repeat-containing RNAs and triplet repeat-interacting proteins in human tissues." Acta Biochimica Polonica 55, no. 1 (January 30, 2008): 1–8. http://dx.doi.org/10.18388/abp.2008_3090.

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Numerous human transcripts contain tandem repeats of trinucleotide motifs, the function of which remains unknown. In this study we used the available gene expression EST data to characterize the abundance of a large group of these transcripts in different tissues and determine the mRNAs which had the highest contribution to the observed levels of transcripts containing different types of the CNG repeats. A more extensive characteristics was performed for transcripts containing the CUG repeats, and those encoding the repeat-binding proteins. The scarcity of double-stranded CUG repeats as well as various proportions of the single-stranded and double-stranded CUG repeat-binding proteins were revealed in the studied transcriptomes. The observed correlated levels of transcripts containing single-stranded CUG repeats and of proteins binding single-stranded CUG repeats may imply that in addition to transcripts which only provide binding sites for these proteins there may be a substantial portion of the transcripts whose metabolism is directly regulated by such proteins. Our results showing a highly variable composition of triplet repeat-containing transcripts and their interacting proteins in different tissues may contribute to a better understanding of the mechanism of RNA-mediated pathogenesis in triplet repeat expansion diseases.

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Peng, Shaohong, Pei Guo, Xiao Lin, Ying An, Kong Hung Sze, Matthew Ho Yan Lau, Zhefan Stephen Chen, et al. "CAG RNAs induce DNA damage and apoptosis by silencing NUDT16 expression in polyglutamine degeneration." Proceedings of the National Academy of Sciences 118, no. 19 (May 4, 2021): e2022940118. http://dx.doi.org/10.1073/pnas.2022940118.

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DNA damage plays a central role in the cellular pathogenesis of polyglutamine (polyQ) diseases, including Huntington’s disease (HD). In this study, we showed that the expression of untranslatable expanded CAG RNA per se induced the cellular DNA damage response pathway. By means of RNA sequencing (RNA-seq), we found that expression of the Nudix hydrolase 16 (NUDT16) gene was down-regulated in mutant CAG RNA-expressing cells. The loss of NUDT16 function results in a misincorporation of damaging nucleotides into DNAs and leads to DNA damage. We showed that small CAG (sCAG) RNAs, species generated from expanded CAG transcripts, hybridize with CUG-containing NUDT16 mRNA and form a CAG-CUG RNA heteroduplex, resulting in gene silencing of NUDT16 and leading to the DNA damage and cellular apoptosis. These results were further validated using expanded CAG RNA-expressing mouse primary neurons and in vivo R6/2 HD transgenic mice. Moreover, we identified a bisamidinium compound, DB213, that interacts specifically with the major groove of the CAG RNA homoduplex and disfavors the CAG-CUG heteroduplex formation. This action subsequently mitigated RNA-induced silencing complex (RISC)-dependent NUDT16 silencing in both in vitro cell and in vivo mouse disease models. After DB213 treatment, DNA damage, apoptosis, and locomotor defects were rescued in HD mice. This work establishes NUDT16 deficiency by CAG repeat RNAs as a pathogenic mechanism of polyQ diseases and as a potential therapeutic direction for HD and other polyQ diseases.

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Chang, Elizabeth T., James M. Donahue, Lan Xiao, Yuhong Cui, Jaladanki N. Rao, Douglas J. Turner, William S. Twaddell, Jian-Ying Wang, and Richard J. Battafarano. "The RNA-binding protein CUG-BP1 increases survivin expression in oesophageal cancer cells through enhanced mRNA stability." Biochemical Journal 446, no. 1 (July 27, 2012): 113–23. http://dx.doi.org/10.1042/bj20120112.

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Survivin, a member of the IAP (inhibitor of apoptosis protein) family, plays important roles in maintaining cellular homoeostasis and regulating cell-cycle progression. This IAP is overexpressed in oesophageal cancer cells, leading to uncontrolled cell growth and resistance to apoptosis. CUG-BP1 (CUG-binding protein 1) is an RNA-binding protein that regulates the stability and translational efficiency of target mRNAs. In the present paper, we report that CUG-BP1 is overexpressed in oesophageal cancer cell lines and human oesophageal cancer specimens. CUG-BP1 associates with the 3′-untranslated region of survivin mRNA, thereby stabilizing the transcript and elevating its expression in oesophageal cancer cells. Our results show that overexpression of CUG-BP1 in oesophageal epithelial cells results in increased survivin mRNA stability and consequently survivin protein expression. Conversely, silencing CUG-BP1 in oesophageal cancer cells destabilizes survivin mRNA, lowering the level of survivin protein. In addition, we have found that altering CUG-BP1 expression modulates susceptibility to chemotherapy-induced apoptosis. Overexpression of CUG-BP1 in oesophageal epithelial cells increases resistance to apoptosis, whereas silencing CUG-BP1 makes oesophageal cancer cells more susceptible to chemotherapy-induced apoptosis. Co-transfection experiments with small interfering RNA directed against survivin suggest that the anti-apoptotic role for CUG-BP1 is not entirely dependent on its effect on survivin expression.

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Sha, Zongyao, Yahya Ali, Yuwei Wang, Jiangping Chen, Xicheng Tan, and Ruren Li. "Mapping the Changes in Urban Greenness Based on Localized Spatial Association Analysis under Temporal Context Using MODIS Data." ISPRS International Journal of Geo-Information 7, no. 10 (October 13, 2018): 407. http://dx.doi.org/10.3390/ijgi7100407.

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Vegetation plays an irreplaceable role for urban ecosystem services. Urban greenness represents all vegetation cover in and around cities. Understanding spatiotemporal patterns of the changes in urban greenness (CUG) provides fundamental clues for urban planning. The impact on CUG can be roughly categorized as being climate-induced and human-induced. Methods for mapping human-induced CUG (H-CUG) are rare. In this paper, a new framework, known as Localized Spatial Association Analysis under Temporal Context (LSAA-TC), was proposed to explore H-CUG. Localized spatial association analysis (LSAA) was performed first to extract local spatial outliers (LSOs), or locations that differ significantly in urban greenness from those located in the neighborhood. LSOs were then analyzed under the temporal context to map their intertemporal variations known as spatiotemporal outliers. We applied LSAA-TC to mapping H-CUG in the Wuhan Metropolitan Area, China during 2000–2015 using the vegetation index from Moderate-resolution Imaging Spectroradiometer (MODIS) 13Q1 as the proxy for urban greenness. The computed H-CUG demonstrated apparent spatiotemporal patterns. The result is consistent with the fact that the traditional downtown area presents the lowest H-CUG, while it is found that the peripheral area in the circular belt within 14–20 km from the urban center demonstrates the most significant H-CUG. We conclude that LSAA-TC can be a widely applicable framework to understand H-CUG patterns and is a promising tool for informative urban planning.

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Sun, Jinguo, Yucun Liu, Longyi Jin, Tie Chen, and Bingzhu Yin. "Coordination-induced gelation of an l-glutamic acid Schiff base derivative: the anion effect and cyanide-specific selectivity." Chemical Communications 52, no. 4 (2016): 768–71. http://dx.doi.org/10.1039/c5cc07903a.

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Three metallogels, ZnG, CuG and Zn-CuG, were prepared in the presence of specific anions, with their efficacy linked to the Hofmeister series. Importantly, Zn-CuG gel could fluorescently detect CN⁻ with specific selectivity.

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Krukowski, Jakub, Adam Kałużny, Jakub Kłącz, and Marcin Matuszewski. "Comparison between cystourethrography and sonourethrography in preoperative diagnostic management of patients with anterior urethral strictures." Medical Ultrasonography 20, no. 4 (December 8, 2018): 436. http://dx.doi.org/10.11152/mu-1613.

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Aim: To evaluate the urethral lesions and the degree of spongiofibrosis using cystourethrography (CUG) and sonourethrography (SUG) in order to propose the best imaging method for further surgical treatment.Material and methods: The study involved 66 patients with anterior urethral strictures with indication for urethroplasty. Results of CUG and SUG were compared with each other and data from surgical protocol.Results: Totally 72 strictures were detected; 47 in the bulbar part of urethra and 25 in the penile urethra. The mean length of the stenosis was 16.43 mm for CUG and 27.41 mm for SUG and 31.05 mm during surgery. The correlation levels between imaging techniques and intraoperative measurements were 0.55 (p<0.001) for CUG and 0.73 (p<0.001) for SUG. After dividing the strictures according to their location, better correlation for stenoses was obtained in penile urethra: 0.66 (p<0.001) for CUG and 0.86 (p<0.001) for SUG.Conclusions: SUG seems to be a simple and fast examination to evaluate urethral strictures. It is more accurate in comparison to CUG and gives a possibility to assess the spongiofibrosis. This information suggests that SUG can be a good complement to CUG in diagnosis of anterior urethtral strictures.

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Dissertations / Theses on the topic "CUG"

1

Chukeatirote, Ekachai. "Evolution of CUG codon reassignment in Candida species." Thesis, University of Kent, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.300944.

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Gromak, Natalia. "The role of CUG-repeat RNA elements and CUG-binding proteins in the regulation of α-actinin and α-tropomyosin alternative splicing." Thesis, University of Cambridge, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.620151.

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Delorimier, Elaine. "Structure-Stabilizing RNA Modifications Prevent MBNL Binding to Toxic CUG and CCUG Repeat RNA in Myotonic Dystrophy." Thesis, University of Oregon, 2015. http://hdl.handle.net/1794/19313.

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Myotonic dystrophy is a genetic neurodegenerative disease caused by repeat expansion mutations. Myotonic dystrophy type 1 (DM1) is caused by a CTG repeat expansion in the 3’ UTR of the dystrophia myotonia protein kinase (DMPK) gene, while myotonic dystrophy type 2 (DM2) is caused by a CCTG repeat expansion in intron 1 of the zinc finger protein nine (Znf9) gene. When expressed, these genes produce long CUG/CCUG repeat RNAs that bind and sequester a family of RNA-binding proteins known as muscleblind-like 1, 2 and 3 (MBNL1, MBNL2, MBNL3). Sequestration of these proteins plays a prominent role in pathogenicity in myotonic dystrophy. MBNL proteins regulate alternative splicing, and myotonic dystrophy symptoms are a result of mis-spliced transcripts that MBNL proteins regulate. MBNL proteins bind to a consensus sequence YGCY (Y = pyrimidine), which is found in CUG and CCUG repeats, and cellular RNA substrates that MBNL proteins bind and regulate. CUG and CCUG repeats can form A-form helices, however it is hypothesized that MBNL proteins bind to the helices when they are open and the YGCY binding site is single-stranded in nature. To evaluate this hypothesis, we used structure-stabilizing RNA modifications pseudouridine (Ψ) and 2’-O-methylation to determine if stabilization of CUG and CCUG repeat helices affected MBNL1 binding and toxicity. We also used Ψ to determine if the structure-stabilizing modification affected MBNL binding to single-stranded YGCY RNA. CUG repeats modified with Ψ or 2’-O-methyl groups exhibited enhanced structural stability and reduced affinity for MBNL1. Ψ also stabilized the structure of CCUG repeats and rigidified single-stranded YGCY RNA and inhibited MBNL1 binding to both of these RNAs. Binding data from CCUG repeats and single-stranded YGCY RNA suggest that both pyrimidines in the YGCY motif must be modified for significant inhibition. Molecular dynamics and X-ray crystallography suggest a potential water-bridging mechanism for Ψ-mediated CUG repeat stabilization. Molecular dynamics simulations suggest that Ψ increases base-stacking interactions, and reducing the flexibility of single-stranded RNA leads to reduced MBNL1 binding. Ψ modification rescued mis-splicing in a cellular DM1 model and prevented CUG repeat toxicity in zebrafish embryos. This dissertation includes previously published and unpublished coauthored material.

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Truong, Brian. "Myotonic dystrophy : the structure of CUG repeats in solution /." view abstract or download text of file, 2007. http://hdl.handle.net/1794/3958.

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Sun, Guangping. "Chromatin condensation and fragmentation caused by CUG-initiated FGF-2 in cardiomyocytes." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0023/MQ51803.pdf.

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Siboni, Ruth. "Characterization of Small Molecules that Reduce CUG Repeat RNA in Myotonic Dystrophy." Thesis, University of Oregon, 2015. http://hdl.handle.net/1794/19260.

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Myotonic dystrophy (DM) is an inherited disease characterized by myotonia, insulin resistance, cardiomyopathy, and cognitive deficiencies. DM is a triplet repeat disorder, meaning that affected individuals carry anywhere between 50 and thousands of CTG/CCTG repeats in their genetic makeup. When transcribed into RNA, these repeats become “toxic” in the sense that they serve to bind and sequester important RNA binding proteins. One such family of proteins, the Muscleblind-like (MBNL) family, is important in the regulation of alternative mRNA splicing, and thus the sequestration of MBNL proteins leads to a number of mis-splicing events. Many of these events are directly correlated to DM symptoms. While there is no known cure for DM, the use of small molecules to treat symptoms is a well-characterized therapeutic tactic with immense promise. Pentamidine is a small molecule that was found to reverse mis-splicing in both DM cell and mouse models. Mechanistically, this molecule is particularly unique because unlike many small molecules, which physically displace MBNL from the toxic CUG RNA, pentamidine reduces CUG RNA levels, possibly through inhibition of CTG transcription. Chapter I summarizes alternative splicing mechanisms and regulation, defines MBNL protein structure and function, describes DM pathophysiology and molecular mechanism, and finally provides an overview of pentamidine characterization as a small molecule therapeutic. Chapter II reports the development of an in vitro T7 transcription assay, which allowed us to compare the relative efficacy by which pentamidine is able to inhibit the transcription of various repeat and non-repeat DNA sequences. This chapter further reports the characterization of a series of methylene linker analogues of pentamidine, which were also characterized through the T7 transcription assay. Chapter III details our thorough structure-activity relationship investigation of bisbenzamidine analogues of pentamidine, both in in vivo and in vitro models. Chapter IV describes our characterization of actinomycin D, a known transcription inhibitor and chemotherapeutic, within the DM disease framework. Chapter V summarizes these data, which ultimately serve as a proof of concept for the potential of CTG transcription inhibition in therapeutic contexts and broadly describe their application in other repeat diseases. This dissertation contains previously published and unpublished co-authored material.
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WIlburn, Brian P. "Expression of bidirectional CUG/CAG transcripts and polyglutamine mediated interference of CREB-binding protein function in a mouse model of Huntington's disease like-2." Diss., Restricted to subscribing institutions, 2008. http://proquest.umi.com/pqdweb?did=1779835091&sid=4&Fmt=2&clientId=1564&RQT=309&VName=PQD.

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Matlin, Arianne Jane. "Regulation of α-actinin alternative splicing by polypyrimidine tract binding protein and CUG binding proteins." Thesis, University of Cambridge, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.614724.

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Le, Mée Gwenn. "Protéines de liaison à l'ARN et toxicité des ARN portant des expansions CUG chez la drosophile." Montpellier 1, 2007. http://www.theses.fr/2007MON1T010.

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La DM1 est une maladie génétique liée à des expansions de triplets CTG dans la région 3'UTR du gène de la myotonine protéine kinase (le gène dmpk). Le nombre de répétitions, inférieur à 37 chez un sujet sain, peut atteindre plusieurs milliers dans les formes sévères. L'ARN dmpk muté portant les expansions CUG, sous forme de structure double brin, s'accumule dans les noyaux sous forme de foyers. Plusieurs arguments suggèrent un effet toxique de l'ARN par séquestration de protéines de liaison à l'ARN double brin comme les protéines MBNL homologues des protéines Muscleblind de drosophile. En outre, l'activité de la protéine CUG-BP1 de liaison aux répétitions CUG est affectée. Mon travail de thèse a porté tout d'abord sur l'identification et la caractérisation du facteur de drosophile homologue de la CUG-BP1 (Delaunay et al. , NAR 2004). Les acteurs de la DM1 sont donc conservés entre la drosophile et l'homme. En raison de cette conservation, la deuxième partie de mes travaux de thèse a porté précisément sur la réalisation de modèles drosophile pour la DM1. Le but de ce travail est d'analyser les mécanismes moléculaires de la pathogénicité des expansions CTG et en particulier de vérifier l'hypothèse de la toxicité des ARN portant des expansions CUG. Des lignées de drosophiles transgéniques ont donc été réalisées en utilisant le système UAS/Gal4 qui permet de contrôler spacio-temporellement l'expression de l'ARN transgénique. Comme chez l'homme, dans tous les tissus observés où leur expression est induite, les expansions CUG240 et 480 forment des foyers nucléaires. Pourtant, parmi sept lignées différentes, la toxicité n'est observée que dans une seule lignée CTG240. Une analyse moléculaire a donc été menée afin d'identifier le mécanisme qui permet de rendre compte de ces différences. En conclusion de ces travaux, nous pouvons affirmer que les expansions CUG ne sont pas toxiques par elles-mêmes quelle que soit leur taille. En outre, les différences de niveau des ARN CUGn produits ne se traduisent pas par des différences de toxicité. Le facteur déterminant de la toxicité semble être lié au contexte dans lequel l'expansion est insérée.

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Barreau, Carine. "Étude fonctionnelle des éléments riches en AU de type III et implication de la protéine CUG-BP1." Rennes 1, 2005. http://www.theses.fr/2005REN1S055.

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Les éléments riches en AU (AU-rich element, ARE) sont des séquences localisées dans la région 3' non traduite (3'UTR) d'ARNm mammifères instables. Par transfection de cellules mammifères, nous avons démontré que la présence de l'ARE du proto-oncogène c-jun (classe III) ou d'une séquence EDEN stimule la traduction tout en déstabilisant un ARNm rapporteur. Les résultats, obtenus par "adressage" de la protéine CUG-BP1 sur un ARNm rapporteur et par inhibition de l'expression de la CUG-BP1 par interférence à l'ARN, impliquent la CUG-BP1 dans ce double effet de déstabilisation et de stimulation traductionnelle causé par un ARE de classe III. L'ensemble de ces données révèle une importante complexité des régulations post-transcriptionnelles de l'expression des gènes liées aux ARE de classe III.

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Books on the topic "CUG"

1

1881-1948, Garcia-Junceda Joan Enric, ed. Junceda. Barcelona: Àmbit, 2013.

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Kawauchi, Rinko. Cui cui. Tokyo: Foil, 2005.

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Snodaigh, Padraig O. Cul le Cul. Baile Atha Cliath: Coisceim, 1988.

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Fowler, Allan. Cua, cua, gra, gra! Chicago, IL: Childrens Press, 1993.

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Cud. Wołowiec: Wyd. Czarne, 2007.

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Danielle, Steel. Cud. Słupsk: Oxford Educational, 2009.

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Karpowicz, Ignacy. Cud. Wolowiec: Wydawnictwo "Czarne", 2007.

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Cud. Kraków: Wydawnictwo Literackie, 2013.

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Cog. Multān: Jhok Pablisharz, 2012.

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Cog. Bowie, MD: Dog Star Books, 2013.

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Book chapters on the topic "CUG"

1

Ambulos, Nicholas P., and Paul S. Lovett. "Translation Initiation from a Cug Codon in Bacillus subtilis." In Biotechnology and Environmental Science, 175–78. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-0-585-32386-2_22.

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van Cruchten, Remco T. P., and Derick G. Wansink. "In Vitro Synthesis and RNA Structure Probing of CUG Triplet Repeat RNA." In Methods in Molecular Biology, 187–202. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9784-8_12.

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Balboni, Marco, Sabrina Colombari, and Tullia Gallina Toschi. "Guarantee Committee for Equal Opportunity, Employee Well-Being and Non-discrimination at Work (CUG)." In Health and Gender, 289–93. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-15038-9_30.

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Hirst, Cheryl J. A., Meenhard Herlyn, Peter A. Cattini, and Elissavet Kardami. "High levels of CUG-initiated FGF-2 expression cause chromatin compaction, decreased cardiomyocyte mitosis, and cell death." In Vascular Biochemistry, 111–16. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4615-0298-2_16.

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Patterson, Janet. "Cue." In Encyclopedia of Clinical Neuropsychology, 1017–18. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-57111-9_878.

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Dayma, Kunal, and Vegesna Radha. "C3G." In Encyclopedia of Signaling Molecules, 618–26. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_101544.

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Villars, P., K. Cenzual, J. Daams, R. Gladyshevskii, O. Shcherban, V. Dubenskyy, N. Melnichenko-Koblyuk, et al. "CuI." In Structure Types. Part 5: Space Groups (173) P63 - (166) R-3m, 492. Berlin, Heidelberg: Springer Berlin Heidelberg, 2007. http://dx.doi.org/10.1007/978-3-540-46933-9_382.

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Villars, P., K. Cenzual, J. Daams, R. Gladyshevskii, O. Shcherban, V. Dubenskyy, N. Melnichenko-Koblyuk, et al. "CuI." In Structure Types. Part 5: Space Groups (173) P63 - (166) R-3m, 627. Berlin, Heidelberg: Springer Berlin Heidelberg, 2007. http://dx.doi.org/10.1007/978-3-540-46933-9_507.

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Posypaiko, V. I., and E. A. Alekseeva. "CuI." In Phase Equilibria in Binary Halides, 163–64. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4684-9024-4_46.

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Villars, P., K. Cenzual, J. Daams, R. Gladyshevskii, O. Shcherban, V. Dubenskyy, V. Kuprysyuk, O. Pavlyuk, I. Savysyuk, and S. Stoyko. "CuI." In Structure Types. Part 7: Space Groups (160) R3m - (156) P3m1, 744. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-69949-1_311.

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Conference papers on the topic "CUG"

1

Tojo, Satoshi. "Free-ordered CUG on Chemical Abstract Machine." In the 15th conference. Morristown, NJ, USA: Association for Computational Linguistics, 1994. http://dx.doi.org/10.3115/991250.991288.

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Park, So-Hyun, Young-Ho Park, Aziz Nasridinov, and Joo-Yeoun Lee. "A Person Identification Method in CUG Using Voice Pitch Analysis." In 2014 IEEE International Conference on Big Data and Cloud Computing (BdCloud). IEEE, 2014. http://dx.doi.org/10.1109/bdcloud.2014.132.

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Liu, Yuqing, Jundong Hou, Rei Guo, Danxia Song, and Haiyan Ma. "Research on CUG-HBSC Base of Business Administration Practical Teaching." In 2011 International Conference on Management and Service Science (MASS 2011). IEEE, 2011. http://dx.doi.org/10.1109/icmss.2011.5999236.

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Lee, Kun Yeong, Hong-Gyum Kim, Joohyun Ryu, Do Young Lim, Hanyong Chen, Ann M. Bode, and Zigang Dong. "Abstract 549: The CUG-translated WT1, not AUG-WT1, is an oncogene." In 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.am2018-549.

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Wang, Huilian. "GPR work in China: in commemoration of the 10th anniversary of the CUG GPR activity." In 8th International Conference on Ground Penetrating Radar, edited by David A. Noon, Glen F. Stickley, and Dennis Longstaff. SPIE, 2000. http://dx.doi.org/10.1117/12.383599.

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Aoki, Y., S. Yatsu, S. Oikawa, H. Kitagawa, M. Yagi, N. Kayukawa, B. Tuchida, et al. "Experiments on a SiC-CuG₁-Cu insulator and a construction of 5 MWt long duration MHD channel." In 1990 Plasma Science IEEE Conference Record - Abstracts. IEEE, 1990. http://dx.doi.org/10.1109/plasma.1990.110875.

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Phatak, Pornima, Daniel Mansour, Kimberly Byrnes, Shan Cao, Lan Liu, Ruiyun Li, Rao Jaladanki, Douglas J. Tuner, Jian Ying Wang, and James M. Donahue. "Abstract B227: Overexpression of microRNA 214-3p in esophageal cancer cells enhances sensitivity to chemotherapy-induced apoptosis by targeting CUG-binding protein 1 (CUGBP1) and survivin." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Oct 19-23, 2013; Boston, MA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1535-7163.targ-13-b227.

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Lima, Flávia, and Gilson Lima. "Modelagem CUG coletiva: o princípio colaborativo como um caminho para estimativas de custos de obras preci- sas, ágeis e rastreáveis ainda nas fases iniciais do desenvolvimento dos projetos." In 14ª Conferência Internacional da LARES. Latin American Real Estate Society, 2014. http://dx.doi.org/10.15396/lares_2014_927-1178-1-rv.

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Heraty, Laura, and Vincent Dion. "C03 FAN1 prevents crispr-CAS9 nickase-induced contractions of CAG/CTG repeats." In EHDN Abstracts 2021. BMJ Publishing Group Ltd, 2021. http://dx.doi.org/10.1136/jnnp-2021-ehdn.27.

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Morris, W. G. "CCG." In the ACM SIGPLAN 1991 conference. New York, New York, USA: ACM Press, 1991. http://dx.doi.org/10.1145/113445.113450.

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Reports on the topic "CUG"

1

Lin, Shu Hwa, and Liezel Pagala. Diamond Cut Dress. Ames: Iowa State University, Digital Repository, September 2016. http://dx.doi.org/10.31274/itaa_proceedings-180814-1609.

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Kumar, Srinath Shiv, Dulcy M. Abraham, Hamed Zamenian, Bhavik Ranka, and Prieston Lobo. Warranty Utility Cut Repairs (QC/QA of Utility Cut Repairs). Purdue University, March 2019. http://dx.doi.org/10.5703/1288284316780.

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Biraud, S. CCG-Flasks Instrument Handbook. Office of Scientific and Technical Information (OSTI), March 2016. http://dx.doi.org/10.2172/1246166.

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De Geronimo, Gianluigi, and Michael Furey. Low-power CPG ASIC. Office of Scientific and Technical Information (OSTI), October 2009. http://dx.doi.org/10.2172/1001657.

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Lent, E. Alpha Transport in COG. Office of Scientific and Technical Information (OSTI), May 2014. http://dx.doi.org/10.2172/1557049.

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Lent, E., K. Sale, R. Buck, and M. Descalle. COG validation: SINBAD Benchmark Problems. Office of Scientific and Technical Information (OSTI), February 2004. http://dx.doi.org/10.2172/15014008.

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Fernandes, Huston. Faraday's Cup Design and Testing. Office of Scientific and Technical Information (OSTI), June 2015. http://dx.doi.org/10.2172/1505101.

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Brenden, B. B. Test of dip cup instrumentation. Office of Scientific and Technical Information (OSTI), November 1988. http://dx.doi.org/10.2172/6873207.

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Sanehira, Gabrielle, and Ju-Young M. Kang. Collected, Cut and Recreated Dress. Ames: Iowa State University, Digital Repository, November 2015. http://dx.doi.org/10.31274/itaa_proceedings-180814-1207.

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Lent, E. M. Three Analytic Benchmarks in COG. Office of Scientific and Technical Information (OSTI), January 2014. http://dx.doi.org/10.2172/1557031.

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