Bibliografías temáticas / Premature termination codon

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Literatura académica sobre el tema "Premature termination codon"

Autor: Grafiati
Publicado: 4 de junio de 2021
Última modificación: 20 de febrero de 2023

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Artículos de revistas sobre el tema "Premature termination codon"

1

Zinshteyn, Boris, Niladri K. Sinha, Syed Usman Enam, Benjamin Koleske, and Rachel Green. "Translational repression of NMD targets by GIGYF2 and EIF4E2." PLOS Genetics 17, no. 10 (October 19, 2021): e1009813. http://dx.doi.org/10.1371/journal.pgen.1009813.

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Translation of messenger RNAs (mRNAs) with premature termination codons produces truncated proteins with potentially deleterious effects. This is prevented by nonsense-mediated mRNA decay (NMD) of these mRNAs. NMD is triggered by ribosomes terminating upstream of a splice site marked by an exon-junction complex (EJC), but also acts on many mRNAs lacking a splice junction after their termination codon. We developed a genome-wide CRISPR flow cytometry screen to identify regulators of mRNAs with premature termination codons in K562 cells. This screen recovered essentially all core NMD factors and
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2

Yang, Qian, Chien-Hung Yu, Fangzhou Zhao, Yunkun Dang, Cheng Wu, Pancheng Xie, Matthew S. Sachs, and Yi Liu. "eRF1 mediates codon usage effects on mRNA translation efficiency through premature termination at rare codons." Nucleic Acids Research 47, no. 17 (August 14, 2019): 9243–58. http://dx.doi.org/10.1093/nar/gkz710.

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Abstract Codon usage bias is a universal feature of eukaryotic and prokaryotic genomes and plays an important role in regulating gene expression levels. A major role of codon usage is thought to regulate protein expression levels by affecting mRNA translation efficiency, but the underlying mechanism is unclear. By analyzing ribosome profiling results, here we showed that codon usage regulates translation elongation rate and that rare codons are decoded more slowly than common codons in all codon families in Neurospora. Rare codons resulted in ribosome stalling in manners both dependent and ind
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3

Morozov, Igor Y., Susana Negrete-Urtasun, Joan Tilburn, Christine A. Jansen, Mark X. Caddick, and Herbert N. Arst. "Nonsense-Mediated mRNA Decay Mutation in Aspergillus nidulans." Eukaryotic Cell 5, no. 11 (September 8, 2006): 1838–46. http://dx.doi.org/10.1128/ec.00220-06.

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ABSTRACT An Aspergillus nidulans mutation, designated nmdA1, has been selected as a partial suppressor of a frameshift mutation and shown to truncate the homologue of the Saccharomyces cerevisiae nonsense-mediated mRNA decay (NMD) surveillance component Nmd2p/Upf2p. nmdA1 elevates steady-state levels of premature termination codon-containing transcripts, as demonstrated using mutations in genes encoding xanthine dehydrogenase (hxA), urate oxidase (uaZ), the transcription factor mediating regulation of gene expression by ambient pH (pacC), and a protease involved in pH signal transduction (palB
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4

Barker, G. F., and K. Beemon. "Rous sarcoma virus RNA stability requires an open reading frame in the gag gene and sequences downstream of the gag-pol junction." Molecular and Cellular Biology 14, no. 3 (March 1994): 1986–96. http://dx.doi.org/10.1128/mcb.14.3.1986-1996.1994.

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The intracellular accumulation of the unspliced RNA of Rous sarcoma virus was decreased when translation was prematurely terminated by the introduction of nonsense codons within its 5' proximal gene, the gag gene. Subcellular fractionation of transfected cells suggested that nonsense codon-mediated instability occurred in the cytoplasm. Analysis of constructs containing an in-frame deletion in the nucleocapsid domain of gag, which prevents interaction between the Gag protein and viral RNA, showed that an open reading frame extending to approximately 30 nucleotides from the natural gag terminat
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5

Barker, G. F., and K. Beemon. "Rous sarcoma virus RNA stability requires an open reading frame in the gag gene and sequences downstream of the gag-pol junction." Molecular and Cellular Biology 14, no. 3 (March 1994): 1986–96. http://dx.doi.org/10.1128/mcb.14.3.1986.

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The intracellular accumulation of the unspliced RNA of Rous sarcoma virus was decreased when translation was prematurely terminated by the introduction of nonsense codons within its 5' proximal gene, the gag gene. Subcellular fractionation of transfected cells suggested that nonsense codon-mediated instability occurred in the cytoplasm. Analysis of constructs containing an in-frame deletion in the nucleocapsid domain of gag, which prevents interaction between the Gag protein and viral RNA, showed that an open reading frame extending to approximately 30 nucleotides from the natural gag terminat
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6

Cohen, Sarit, Lior Kramarski, Shahar Levi, Noa Deshe, Oshrit Ben David, and Eyal Arbely. "Nonsense mutation-dependent reinitiation of translation in mammalian cells." Nucleic Acids Research 47, no. 12 (May 2, 2019): 6330–38. http://dx.doi.org/10.1093/nar/gkz319.

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AbstractIn-frame stop codons mark the termination of translation. However, post-termination ribosomes can reinitiate translation at downstream AUG codons. In mammals, reinitiation is most efficient when the termination codon is positioned close to the 5′-proximal initiation site and around 78 bases upstream of the reinitiation site. The phenomenon was studied mainly in the context of open reading frames (ORFs) found within the 5′-untranslated region, or polycicstronic viral mRNA. We hypothesized that reinitiation of translation following nonsense mutations within the main ORF of p53 can promot
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7

Muhlrad, Denise, and Roy Parker. "Recognition of Yeast mRNAs as “Nonsense Containing” Leads to Both Inhibition of mRNA Translation and mRNA Degradation: Implications for the Control of mRNA Decapping." Molecular Biology of the Cell 10, no. 11 (November 1999): 3971–78. http://dx.doi.org/10.1091/mbc.10.11.3971.

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A critical step in the degradation of many eukaryotic mRNAs is a decapping reaction that exposes the transcript to 5′ to 3′ exonucleolytic degradation. The dual role of the cap structure as a target of mRNA degradation and as the site of assembly of translation initiation factors has led to the hypothesis that the rate of decapping would be specified by the status of the cap binding complex. This model makes the prediction that signals that promote mRNA decapping should also alter translation. To test this hypothesis, we examined the decapping triggered by premature termination codons to deter
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8

Daar, I. O., and L. E. Maquat. "Premature translation termination mediates triosephosphate isomerase mRNA degradation." Molecular and Cellular Biology 8, no. 2 (February 1988): 802–13. http://dx.doi.org/10.1128/mcb.8.2.802-813.1988.

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We characterized an anemia-inducing mutation in the human gene for triosephosphate isomerase (TPI) that resulted in the production of prematurely terminated protein and mRNA with a reduced cytoplasmic half-life. The mutation converted a CGA arginine codon to a TGA nonsense codon and generated a protein of 188 amino acids, instead of the usual 248 amino acids. To determine how mRNA primary structure and translation influence mRNA stability, in vitro-mutagenized TPI alleles were introduced into cultured L cells and analyzed for their effect on TPI RNA metabolism. Results indicated that mRNA stab
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9

Daar, I. O., and L. E. Maquat. "Premature translation termination mediates triosephosphate isomerase mRNA degradation." Molecular and Cellular Biology 8, no. 2 (February 1988): 802–13. http://dx.doi.org/10.1128/mcb.8.2.802.

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We characterized an anemia-inducing mutation in the human gene for triosephosphate isomerase (TPI) that resulted in the production of prematurely terminated protein and mRNA with a reduced cytoplasmic half-life. The mutation converted a CGA arginine codon to a TGA nonsense codon and generated a protein of 188 amino acids, instead of the usual 248 amino acids. To determine how mRNA primary structure and translation influence mRNA stability, in vitro-mutagenized TPI alleles were introduced into cultured L cells and analyzed for their effect on TPI RNA metabolism. Results indicated that mRNA stab
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10

Hwang, Jungwook, and Yoon Ki Kim. "When a ribosome encounters a premature termination codon." BMB Reports 46, no. 1 (January 31, 2013): 9–16. http://dx.doi.org/10.5483/bmbrep.2013.46.1.002.

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Tesis sobre el tema "Premature termination codon"

1

Bugaud, Olivier. "Suppression traductionnelle des codons stop chez les mammifères." Thesis, Université Paris-Saclay (ComUE), 2016. http://www.theses.fr/2016SACLS222.

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Entre 10% et 30% des maladies humaines sont liées à l'apparition d'une mutation non-sens (PTC). La synthèse protéique est alors arrêté prématurément. Cet arrêt peut être inhibé par des molécules inductrices de translecture qui permettent l’incorporation d’un ARNt suppresseur naturel au niveau du PTC (translecture). Le ribosome peut alors franchir le PTC et restaurer l’expression de la protéine.Au cours de ma thèse, je me suis intéressé à la suppression des codons stop en caractérisant de nouvelles molécules inductrices de translecture et en analysant les mécanismes de la fidélité de la traduct
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2

Wetterbom, Anna. "Genome and Transcriptome Comparisons between Human and Chimpanzee." Doctoral thesis, Uppsala universitet, Genomik, 2010. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-112893.

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The chimpanzee is humankind’s closest living relative and the two species diverged ~6 million years ago. Comparative studies of the human and chimpanzee genomes and transcriptomes are of great interest to understand the molecular mechanisms of speciation and the development of species-specific traits. The aim of this thesis is to characterize differences between the two species with regard to their genome sequences and the resulting transcript profiles. The first two papers focus on indel divergence and in particular, indels causing premature termination codons (PTCs) in 8% of the chimpanzee g
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3

Maxwell, Megan Amanda, and n/a. "PEX1 Mutations in Australasian Patients with Disorders of Peroxisome Biogenesis." Griffith University. School of Biomolecular and Biomedical Science, 2004. http://www4.gu.edu.au:8080/adt-root/public/adt-QGU20040219.100649.

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The peroxisome is a subcellular organelle that carries out a diverse range of metabolic functions, including the b-oxidation of very long chain fatty acids, the breakdown of peroxide and the a-oxidation of fatty acids. Disruption of peroxisome metabolic functions leads to severe disease in humans. These diseases can be broadly grouped into two categories: those in which a single enzyme is defective, and those known as the peroxisome biogenesis disorders (PBDs), which result from a generalised failure to import peroxisomal matrix proteins (and consequently result in disruption of multiple metab
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4

Maxwell, Megan Amanda. "PEX1 Mutations in Australasian Patients with Disorders of Peroxisome Biogenesis." Thesis, Griffith University, 2004. http://hdl.handle.net/10072/366184.

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The peroxisome is a subcellular organelle that carries out a diverse range of metabolic functions, including the b-oxidation of very long chain fatty acids, the breakdown of peroxide and the a-oxidation of fatty acids. Disruption of peroxisome metabolic functions leads to severe disease in humans. These diseases can be broadly grouped into two categories: those in which a single enzyme is defective, and those known as the peroxisome biogenesis disorders (PBDs), which result from a generalised failure to import peroxisomal matrix proteins (and consequently result in disruption of multiple metab
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5

Benhabiles, Hana. "Etude de la correction de mutations non sens par de nouvelles molécules pouvant servir d'approches thérapeutiques ciblées." Thesis, Lille 2, 2017. http://www.theses.fr/2017LIL2S046.

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Les mutations non sens introduisent un codon stop prématuré dans une phase ouverte de lecture. Ce type de mutation est retrouvé chez environ 11% des patients atteints de maladies génétiques et dans de nombreux cancers. En effet, entre 5 et 40% des mutations affectant des gènes suppresseurs de tumeurs sont des mutations non sens. La conséquence de la présence d’une mutation non sens dans un gène est la dégradation rapide de l’ARN messager correspondant, par l’activation d’un mécanisme de surveillance des ARN appelé NMD (pour nonsense-mediated mRNA decay) conduisant à une absence d’expression du
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6

Yngvadóttir, Bryndís. "Evolution by gene loss? : a genome-wide survey of human SNPs that introduce premature termination codons." Thesis, University of Cambridge, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.611311.

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Actas de conferencias sobre el tema "Premature termination codon"

1

Yoon, SeongJu, Won Kyu Kim, Jeon Han Park, and Hoguen Kim. "Abstract 2416: Protein expression analysis of premature termination codon containing mutant proteins in colon cancers with high microsatellite instability." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-2416.

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