Academic literature on the topic 'Premature termination codon'
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Journal articles on the topic "Premature termination codon"
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.
Full textYang, 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.
Full textMorozov, 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.
Full textBarker, 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.
Full textBarker, 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.
Full textCohen, 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.
Full textMuhlrad, 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.
Full textDaar, 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.
Full textDaar, 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.
Full textHwang, 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.
Full textDissertations / Theses on the topic "Premature termination codon"
Bugaud, Olivier. "Suppression traductionnelle des codons stop chez les mammifères." Thesis, Université Paris-Saclay (ComUE), 2016. http://www.theses.fr/2016SACLS222.
Full textNonsense mutations, also known as premature termination codons (PTCs) are responsible for 10% to 30% of all human genetic diseases. Nonsense translation suppression can be induced by readthrough inducers. The presence of such PTC leads to premature translation termination. These stop therapeutic strategies have emerged which attempt to use molecules that facilitate tRNA incorporation at the PTC (readthrough). The, translation continue in the same reading frame until the next stop codon. I first developed an innovative screening system I used to test more than 17,000 molecules and have identified one hit, TLN468 molecule. I have shown that this molecule is able to induce re-expression of an active p53 protein.I also characterized new compounds derived from aminoglycosides. I have shown that the NB124 induces apoptosis of tumor cells by re-expressing p53 protein while having a much lower toxicity than gentamicin.I developed a single molecule approach for studying the ribosome programmed errors (recoding). I was able to analyze the kinetics of elongation eukaryotic ribosomes and showed that the initiation of translation at an internal entry site (IRES) slows the ribosome during the first elongation cycle
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.
Full textMaxwell, 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.
Full textMaxwell, Megan Amanda. "PEX1 Mutations in Australasian Patients with Disorders of Peroxisome Biogenesis." Thesis, Griffith University, 2004. http://hdl.handle.net/10072/366184.
Full textThesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Biomolecular and Biomedical Sciences
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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.
Full textNonsense mutations generate premature termination codons (PTC) within an open reading frame. This type of mutation is found in about 11% of patients with genetic disorders. Concerning cancer, 5 to 40% of mutations affecting tumor-suppressing genes are nonsense mutations. The presence of a PTC in a gene leads to rapid degradation of its mRNA mediated by the RNA surveillance mechanism named NMD (Nonsense-mediated mRNA decay) preventing the synthesis of truncated proteins. In cancer, the absence of expression of tumor suppressing genes such as TP53 interferes with many biological pathways including apoptosis enabling tumor progression.A screening system that allows identifying molecules capable of re-expressing genes harboring nonsense mutations by inhibiting the NMD system and/or by activating readthrough has been developed in the lab. Readthrough is a natural mechanism, which occurs during translation, leading to the incorporation of an amino acid at the PTC position. Among the molecules that have been identified thanks to the screen, a natural extract named H7 and a compound named CNSM1 efficiently rescues the expression of the nonsense-mutated TP53 gene carrying a PTC.CNSM1 and H7 induces the expression of full-length proteins from PTC-containing genes indicating that these compounds are capable of activating readthrough. I validated the screen results on several cancer cell lines harboring an endogenous nonsense mutation in TP53 gene and showed that the function of p53 was restored in the presence of CNSM1 or H7. I also investigated the cellular toxicity related with the use of CMNS1 on cultured cells and the in vivo effect of H7 in a mouse model harboring a nonsense mutation in dystrophin gene. My results demonstrate that these compounds have a mild cellular toxicity. In addition, using a genome editing approach I confirmed the relationship between the cytoskeletal blockage and the NMD inhibition. I identified two proteins that are implicated in the cytoskeletal rearrangement, which might be targeted to induce NMD inhibition and then the expression of truncated but functional protein from the mutated mRNA. H7 or CNMS1 might be coupled to an NMD inhibition strategy to improve the nonsense mutation correction. Knowing CNSM1 and H7 are so far the most efficient molecule capable of rescuing the expression of PTC-containing genes, these compounds represents a realistic hope for a new-targeted therapy for pathologies associated with nonsense mutations
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.
Full textConference papers on the topic "Premature termination codon"
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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