Relevant bibliographies by topics / NMD

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  2. Dissertations / Theses
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  4. Book chapters
  5. Conference papers
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Academic literature on the topic 'NMD'

Author: Grafiati
Published: 4 June 2021
Last updated: 25 May 2024

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Journal articles on the topic "NMD"

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Domingo, Deepti, Urwah Nawaz, Mark Corbett, Josh L. Espinoza, Katrina Tatton-Brown, David Coman, Miles F. Wilkinson, Jozef Gecz, and Lachlan A. Jolly. "A synonymous UPF3B variant causing a speech disorder implicates NMD as a regulator of neurodevelopmental disorder gene networks." Human Molecular Genetics 29, no. 15 (July 16, 2020): 2568–78. http://dx.doi.org/10.1093/hmg/ddaa151.

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Abstract Loss-of-function mutations of the X-chromosome gene UPF3B cause male neurodevelopmental disorders (NDDs) via largely unknown mechanisms. We investigated initially by interrogating a novel synonymous UPF3B variant in a male with absent speech. In silico and functional studies using cell lines derived from this individual show altered UPF3B RNA splicing. The resulting mRNA species encodes a frame-shifted protein with a premature termination codon (PTC) predicted to elicit degradation via nonsense-mediated mRNA decay (NMD). UPF3B mRNA was reduced in the cell line, and no UPF3B protein was produced, confirming a loss-of-function allele. UPF3B is itself involved in the NMD mechanism which degrades both PTC-bearing mutant transcripts and also many physiological transcripts. RNAseq analysis showed that ~1.6% of mRNAs exhibited altered expression. These mRNA changes overlapped and correlated with those we identified in additional cell lines obtained from individuals harbouring other UPF3B mutations, permitting us to interrogate pathogenic mechanisms of UPF3B-associated NDDs. We identified 102 genes consistently deregulated across all UPF3B mutant cell lines. Of the 51 upregulated genes, 75% contained an NMD-targeting feature, thus identifying high-confidence direct NMD targets. Intriguingly, 22 of the dysregulated genes encoded known NDD genes, suggesting UPF3B-dependent NMD regulates gene networks critical for cognition and behaviour. Indeed, we show that 78.5% of all NDD genes encode a transcript predicted to be targeted by NMD. These data describe the first synonymous UPF3B mutation in a patient with prominent speech and language disabilities and identify plausible mechanisms of pathology downstream of UPF3B mutations involving the deregulation of NDD-gene networks.
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Kim, Eunha, and Jun R. Huh. "NMD Takes the Immune Road to NDD." Neuron 104, no. 4 (November 2019): 625–26. http://dx.doi.org/10.1016/j.neuron.2019.10.042.

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Ghosh, P. K. "Naval NMD: The concept of expanding NMD seawards*." Strategic Analysis 25, no. 8 (November 2001): 897–919. http://dx.doi.org/10.1080/09700160108459007.

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Udy, Dylan B., and Robert K. Bradley. "Nonsense-mediated mRNA decay uses complementary mechanisms to suppress mRNA and protein accumulation." Life Science Alliance 5, no. 3 (December 8, 2021): e202101217. http://dx.doi.org/10.26508/lsa.202101217.

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Nonsense-mediated mRNA decay (NMD) is an essential, highly conserved quality control pathway that detects and degrades mRNAs containing premature termination codons. Although the essentiality of NMD is frequently ascribed to its prevention of truncated protein accumulation, the extent to which NMD actually suppresses proteins encoded by NMD-sensitive transcripts is less well-understood than NMD-mediated suppression of mRNA. Here, we describe a reporter system that permits accurate quantification of both mRNA and protein levels via stable integration of paired reporters encoding NMD-sensitive and NMD-insensitive transcripts into the AAVS1 safe harbor loci in human cells. We use this system to demonstrate that NMD suppresses proteins encoded by NMD-sensitive transcripts by up to eightfold more than the mRNA itself. Our data indicate that NMD limits the accumulation of proteins encoded by NMD substrates by mechanisms beyond mRNA degradation, such that even when NMD-sensitive mRNAs escape destruction, their encoded proteins are still effectively suppressed.
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Sun, Lingling, Justine Mailliot, and Christiane Schaffitzel. "Nonsense-Mediated mRNA Decay Factor Functions in Human Health and Disease." Biomedicines 11, no. 3 (February 27, 2023): 722. http://dx.doi.org/10.3390/biomedicines11030722.

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Nonsense-mediated mRNA decay (NMD) is a cellular surveillance mechanism that degrades mRNAs with a premature stop codon, avoiding the synthesis of C-terminally truncated proteins. In addition to faulty mRNAs, NMD recognises ~10% of endogenous transcripts in human cells and downregulates their expression. The up-frameshift proteins are core NMD factors and are conserved from yeast to human in structure and function. In mammals, NMD diversified into different pathways that target different mRNAs employing additional NMD factors. Here, we review our current understanding of molecular mechanisms and cellular roles of NMD pathways and the involvement of more specialised NMD factors. We describe the consequences of mutations in NMD factors leading to neurodevelopmental diseases, and the role of NMD in cancer. We highlight strategies of RNA viruses to evade recognition and decay by the NMD machinery.
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Peccarelli, Megan, and Bessie W. Kebaara. "Regulation of Natural mRNAs by the Nonsense-Mediated mRNA Decay Pathway." Eukaryotic Cell 13, no. 9 (July 18, 2014): 1126–35. http://dx.doi.org/10.1128/ec.00090-14.

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ABSTRACT The nonsense-mediated mRNA decay (NMD) pathway is a specialized mRNA degradation pathway that degrades select mRNAs. This pathway is conserved in all eukaryotes examined so far, and it triggers the degradation of mRNAs that prematurely terminate translation. Originally identified as a pathway that degrades mRNAs with premature termination codons as a result of errors during transcription, splicing, or damage to the mRNA, NMD is now also recognized as a pathway that degrades some natural mRNAs. The degradation of natural mRNAs by NMD has been identified in multiple eukaryotes, including Saccharomyces cerevisiae , Drosophila melanogaster , Arabidopsis thaliana , and humans. S. cerevisiae is used extensively as a model to study natural mRNA regulation by NMD. Inactivation of the NMD pathway in S. cerevisiae affects approximately 10% of the transcriptome. Similar percentages of natural mRNAs in the D. melanogaster and human transcriptomes are also sensitive to the pathway, indicating that NMD is important for the regulation of gene expression in multiple organisms. NMD can either directly or indirectly regulate the decay rate of natural mRNAs. Direct NMD targets possess NMD-inducing features. This minireview focuses on the regulation of natural mRNAs by the NMD pathway, as well as the features demonstrated to target these mRNAs for decay by the pathway in S. cerevisiae . We also compare NMD-targeting features identified in S. cerevisiae with known NMD-targeting features in other eukaryotic organisms.
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Chen, Chengyan, Yanmin Shen, Luqian Li, Yaoxin Ren, Zhao-Qi Wang, and Tangliang Li. "UPF3A is dispensable for nonsense-mediated mRNA decay in mouse pluripotent and somatic cells." Life Science Alliance 6, no. 6 (March 30, 2023): e202201589. http://dx.doi.org/10.26508/lsa.202201589.

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Nonsense-mediated mRNA decay (NMD) is a highly conserved regulatory mechanism of post-transcriptional gene expression in eukaryotic cells. NMD plays essential roles in mRNA quality and quantity control and thus safeguards multiple biological processes including embryonic stem cell differentiation and organogenesis. UPF3A and UPF3B in vertebrate species, originated from a singleUPF3gene in yeast, are key factors in the NMD machinery. Although UPF3B is a well-recognized weak NMD-promoting factor, whether UPF3A functions in promoting or suppressing NMD is under debate. In this study, we generated aUpf3aconditional knockout mouse strain and established multiple lines of embryonic stem cells and somatic cells without UPF3A. Through extensive analysis on the expressions of 33 NMD targets, we found UPF3A neither represses NMD in mouse embryonic stem cells, somatic cells, nor in major organs including the liver, spleen, and thymus. Our study reinforces that UPF3A is dispensable for NMD when UPF3B is present. Furthermore, UPF3A may weakly and selectively promote NMD in certain murine organs.
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Lloyd, James P. B. "The evolution and diversity of the nonsense-mediated mRNA decay pathway." F1000Research 7 (August 15, 2018): 1299. http://dx.doi.org/10.12688/f1000research.15872.1.

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Nonsense-mediated mRNA decay is a eukaryotic pathway that degrades transcripts with premature termination codons (PTCs). In most eukaryotes, thousands of transcripts are degraded by NMD, including many important regulators of development and stress response pathways. Transcripts can be targeted to NMD by the presence of an upstream ORF or by introduction of a PTC through alternative splicing. Many factors involved in the recognition of PTCs and the destruction of NMD targets have been characterized. While some are highly conserved, others have been repeatedly lost in eukaryotic lineages. Here, I outline the factors involved in NMD, our current understanding of their interactions and how they have evolved. I outline a classification system to describe NMD pathways based on the presence/absence of key NMD factors. These types of NMD pathways exist in multiple different lineages, indicating the plasticity of the NMD pathway through recurrent losses of NMD factors during eukaryotic evolution. By classifying the NMD pathways in this way, gaps in our understanding are revealed, even within well studied organisms. Finally, I discuss the likely driving force behind the origins of the NMD pathway before the appearance of the last eukaryotic common ancestor: transposable element expansion and the consequential origin of introns.
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Lloyd, James P. B. "The evolution and diversity of the nonsense-mediated mRNA decay pathway." F1000Research 7 (November 22, 2018): 1299. http://dx.doi.org/10.12688/f1000research.15872.2.

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Nonsense-mediated mRNA decay is a eukaryotic pathway that degrades transcripts with premature termination codons (PTCs). In most eukaryotes, thousands of transcripts are degraded by NMD, including many important regulators of developmental and stress response pathways. Transcripts can be targeted to NMD by the presence of an upstream ORF or by introduction of a PTC through alternative splicing. Many factors involved in the recognition of PTCs and the destruction of NMD targets have been characterized. While some are highly conserved, others have been repeatedly lost in eukaryotic lineages. Here, I detail the factors involved in NMD, our current understanding of their interactions and how they have evolved. I outline a classification system to describe NMD pathways based on the presence/absence of key NMD factors. These types of NMD pathways exist in multiple different lineages, indicating the plasticity of the NMD pathway through recurrent losses of NMD factors during eukaryotic evolution. By classifying the NMD pathways in this way, gaps in our understanding are revealed, even within well studied organisms. Finally, I discuss the likely driving force behind the origins of the NMD pathway before the appearance of the last eukaryotic common ancestor: transposable element expansion and the consequential origin of introns.
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Echols, Josh, Amna Siddiqui, Yanying Dai, Viktoria Havasi, Richard Sun, Aneta Kaczmarczyk, and Kim M. Keeling. "A regulated NMD mouse model supports NMD inhibition as a viable therapeutic option to treat genetic diseases." Disease Models & Mechanisms 13, no. 8 (July 31, 2020): dmm044891. http://dx.doi.org/10.1242/dmm.044891.

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ABSTRACTNonsense-mediated mRNA decay (NMD) targets mRNAs that contain a premature termination codon (PTC) for degradation, preventing their translation. By altering the expression of PTC-containing mRNAs, NMD modulates the inheritance pattern and severity of genetic diseases. NMD also limits the efficiency of suppressing translation termination at PTCs, an emerging therapeutic approach to treat genetic diseases caused by in-frame PTCs (nonsense mutations). Inhibiting NMD may help rescue partial levels of protein expression. However, it is unclear whether long-term, global NMD attenuation is safe. We hypothesize that a degree of NMD inhibition can be safely tolerated after completion of prenatal development. To test this hypothesis, we generated a novel transgenic mouse that expresses an inducible, dominant-negative form of human UPF1 (dnUPF1) to inhibit NMD in mouse tissues by different degrees, allowing us to examine the effects of global NMD inhibition in vivo. A thorough characterization of these mice indicated that expressing dnUPF1 at levels that promote relatively moderate to strong NMD inhibition in most tissues for a 1-month period produced modest immunological and bone alterations. In contrast, 1 month of dnUPF1 expression to promote more modest NMD inhibition in most tissues did not produce any discernable defects, indicating that moderate global NMD attenuation is generally well tolerated in non-neurological somatic tissues. Importantly, a modest level of NMD inhibition that produced no overt abnormalities was able to significantly enhance in vivo PTC suppression. These results suggest that safe levels of NMD attenuation are likely achievable, and this can help rescue protein deficiencies resulting from PTCs.
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Dissertations / Theses on the topic "NMD"

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Raimondeau, Etienne. "A new link between translation termination and NMD complexes." Thesis, Université Grenoble Alpes (ComUE), 2016. http://www.theses.fr/2016GREAV048/document.

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Environ un tiers des maladies humaines, héréditaires ou acquises, sont dues à la génération d’un codon stop prématuré (PTC). Le système de contrôle appelé dégradation des ARNm non-sens (NMD) permet de détecter puis de dégrader des ARNm contenant un PTC. Les facteurs principaux de la NMD : UPF1, UPF2 et UPF3 reconnaissent les PTCs en interagissant avec le complexe de terminaison de traduction contenant les ribosomes, les facteurs de terminaison eRF1, eRF3 et la protéine poly(A) binding (Pab1p en levure). Nous avons pu résoudre la structure d'un tel complexe en levure comprenant un ribosome en cours de traduction en présence d’un ARNt dans le site P et de facteurs de terminaisons dans le site A. Aucune densité n’a pu être observée pour Pab1p indiquant la flexibilité de l’interaction avec ce complexe. Nous avons aussi évalué l’impact des facteurs de la NMD sur la terminaison dans un système de traduction in vitro humain. UPF3B retarde la reconnaissance du codon stop et favorise la dissociation des sous-unités ribosomales. UPF2 abolit l’effet de UPF3B tandis que l’addition de UPF1 n’a pas d’influence dans la terminaison. Par in vivo et in vitro pulldowns, nous avons montré que UPF3B interagit avec eRF3a et UPF1 et pourrait constituer le lien manquant entre la terminaison et la NMD. Nos résultats illustrent la complexité des mécanismes de la terminaison et de la NMD
Premature termination codons (PTCs) account for approximately one third of inherited and acquired diseases. A surveillance pathway called nonsense-mediated mRNA decay (NMD) detects and degrades PTC-containing transcripts. NMD core factors UPF1, UPF2 and UPF3 mediate the recognition of PTCs by associating with the terminating translation machinery composed of the ribosome, the release factors eRF1 and eRF3 and the poly(A) binding protein (Pab1p in yeast). Using electron cryo-microscopy, we solved such a complex in yeast and observed the translating ribosome, containing a P-site tRNA and an A-site density for the release factors but not for Pab1p indicating that Pab1p is flexibly bound. We also probed the function of NMD factors in mammalian termination using a reconstituted human in vitro translation system. Surprisingly, we found that UPF3B delayed stop codon recognition and promoted ribosomal dissociation. The addition of UPF2 could abolish UPF3B’s effect on translation termination. UPF1 had no influence in the termination process alone or in combination with UPF2. Using in vitro and in vivo pulldowns we found that UPF3B interacts with eRF3a and UPF1, indicating that UPF3B could be the missing link between termination and NMD. Our results point to a complex interplay between the NMD factors and the termination apparatus
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Andjus, Sara. "Role of translation in the degradation of antisense long non-coding RNAs in yeast." Electronic Thesis or Diss., Université Paris sciences et lettres, 2022. http://www.theses.fr/2022UPSLS071.

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Issus de la transcription pervasive des génomes eucaryotes, les longs ARN non codants (nc) sont aujourd’hui reconnus comme des acteurs clés dans divers processus cellulaires. Ils présentent une expression spécifique du tissu ou type cellulaire, et répondent à divers stimuli, suggèrant que leur expression est contrôlée. Leur dérégulation est associée à des maladies humaines, dont le cancer.Parmi les différents longs ARNnc, les ARN antisens (as) sont synthétisés à partir du brin opposé aux gènes codant des protéines. Malgré leur potentiel régulateur, les ARNas restent peu étudiés, à cause de leur faible abondance cellulaire. En fait, chez la levure, ils sont largement dégradés par l'exosome nucléaire et l'exoribonucléase cytoplasmique Xrn1.Des travaux récents menés chez Saccharomyces cerevisiae ont révélé que les ARNas sont ciblés vers Xrn1 par la voie du Nonsense-Mediated mRNA Decay (NMD) qui dépend de la traduction. Cette sensibilité au NMD suggère que les ARNas sont traduits, soulevant la question de leur potentiel codant. D'autre part, les ARNas peuvent former des structures ARN double brin avec les ARNm ‘sens’, les protégeant du NMD. Cependant, les mécanismes moléculaires qui régulent le ciblage des ARNas vers la traduction/dégradation ou l’appariement/stabilisation restent inconnus.Pour mieux comprendre cette problématique, ma thèse visait à étudier la conservation des mécanismes de dégradation dans le contrôle de ARNas, le rôle de la traduction dans ce processus, ainsi que l'hétérogénéité de l’appariement sens/antisens chez la levure.Tout d'abord, nous avons étudié la dégradation des ARNas chez Naumovozyma castellii, qui contrairement à S. cerevisiae contient le système d’interférence par ARN (ARNi), en examinant l'interaction entre l'exosome nucléaire, Xrn1 et la RNase III Dicer. Nos données ont montré que la dégradation des ARNas dans cette espèce dépend de l'exosome nucléaire et de Xrn1, sans effet majeur de Dicer (Szachnowski*, Andjus* et al., 2019). Elles suggèrent également que la présence de la machinerie d'ARNi cytoplasmique chez N. castellii a renforcé le rôle de l’exosome nucléaire pour restreindre l'expression des ARNas.Chez S. cerevisiae, nous avons montré que les ARNas s'accumulent dans des conditions d'inhibition de l’élongation de la traduction, renforçant l'idée que la traduction détermine leur dégradation. Des analyses Ribo-Seq (en collaboration avec le laboratoire du Dr. Namy à l'I2BC, Gif sur Yvette) ont permis de montrer que les ARNas cytoplasmiques sont activement traduits. De plus, nous avons identifié les bases moléculaires qui ciblent les ARNas vers le NMD. Enfin, nous avons montré qu’un peptide est produit à partir d’un ARNas rapporteur sensible au NMD, et est détecté dans des cellules sauvages, alors que ce transcrit est ciblé vers la dégradation via le NMD. Ces résultats sont décrits dans un preprint déposé sur bioRxiv (Andjus et al., 2022), tandis que l'importance évolutive du NMD dans la modulation des ARNnc a fait l'objet de la revue publiée dans Noncoding RNA (Andjus et al., 2021).Enfin, nous avons pu démontrer la large hétérogénéité de la co-expression des ARNm sens/ARNas à l'échelle du génome, en utilisant les données RNA-Seq de cellules uniques (en collaboration avec le laboratoire du Dr. Posas à l'IRB, Barcelone). De plus, nous avons observé une corrélation entre l'augmentation du niveau des ARNas et le nombre de cellules contenant à la fois l’ARNm sens et et son as, soulevant la question de l'impact de la formation de duplex sur le destin des ARN impliqués.En conclusion, mon projet contribue à reconsidérer l'idée que les ARNas sont dépourvus de potentiel codant, mettant en évidence le rôle de la traduction dans leur dégradation via le NMD. Ce travail chez la levure ouvre des perspectives quant à la régulation des ARNas chez les Eucaryotes supérieurs (les facteurs NMD qui les ciblent étant conservés), et quant au rôle régulateur potentiel des peptides dérivés des ARNas
Initially thought to be by-products of the pervasive transcription of eukaryotic genomes, long non-coding (lncRNAs) progressively emerged as key players in multiple cellular processes. LncRNAs show tissue-specific expression and respond to diverse stimuli, suggesting that their expression is precisely controlled. Their dysregulated expression has been associated to human diseases, including cancer. Several classes of lncRNAs exist, including antisense (as)lncRNAs that are synthesized from the strand opposite to sense protein-coding genes. Despite their regulatory importance, aslncRNAs have been poorly explored due to their low cellular abundance. In fact, in yeast they are extensively targeted by RNA decay machineries – nuclear exosome and cytoplasmic Xrn1 exoribonuclease.Recent works in Saccharomyces cerevisiae revealed that aslncRNAs are mainly targeted to Xrn1 through translation-dependent Nonsense-Mediated Decay (NMD) pathway. The NMD-sensitivity of aslncRNAs suggests that they are translated, raising the question of their coding potential. On the other hand, aslncRNAs can also form double-stranded RNA with their paired-sense mRNAs, at least in some cells, protecting them from NMD. However, the extent and the regulatory mechanisms governing the fate of the aslncRNA either subjected to translation/decay or pairing/stabilization are unknown.In this context, to enlighten the metabolism of aslncRNA, the objective of my thesis was to decipher the evolutionary role of decay machineries in controlling aslncRNAs expression, the role of translation in the degradation of aslncRNAs, and the heterogeneity of sense mRNA and aslncRNAs in yeast.First, we studied aslncRNAs degradation in Naumovozyma castellii, a budding yeast endowed with RNAi, unlike S. cerevisiae, which lost it during evolution, by examining the interplay between the nuclear exosome, Xrn1 and the RNase III Dicer. Our data showed that aslncRNAs decay in this species depends on the nuclear exosome and Xrn1 (with no major effect of Dicer) (Szachnowski*, Andjus* et al., 2019). They also suggest that the presence of cytoplasmic RNAi machinery in N. castellii reinforced nuclear RNA surveillance machinery to temper aslncRNAs expression.In S. cerevisiae, we showed that aslncRNAs accumulate upon translation elongation inhibition, reinforcing the idea that translation controls their decay. Using Ribo-Seq (in collaboration with Dr. Namy’s lab at I2BC, Gif sur Yvette) we defined actively translated aslncRNAs. We demonstrated the molecular bases subjecting aslncRNAs to NMD. Finally, we showed that a peptide is produced from an NMD-sensitive aslncRNA reporter, and is detected in wild-type cells, while the transcript is targeted for degradation via NMD. These results are described in a preprint deposited on bioRxiv (Andjus et al., 2022), while the evolutionary importance of NMD in ncRNA modulation was the subject of the review published in Noncoding RNA (Andjus et al., 2021).Lastly, using single-cell RNA-Seq data (in collaboration with Dr. Posas’s lab at IBR, Barcelona), we observed a large heterogeneity of co-expression of sense mRNA/aslncRNAs at the single cell level genome wide, critical for the metabolism of aslncRNAs. Moreover, we showed a direct correlation between aslncRNAs levels and the number of cells containing both sense and as RNA pairs, raising an intriguing hypothesis on the mechanistic impact of duplex formation on the fate of the involving pair.In conclusion, my project contributed to reconsider that aslncRNAs are devoid of coding potential, highlighting the role of translation in determining their degradation via the NMD. As the NMD factors targeting them are conserved, this work in yeast helps comprehend the aslncRNAs metabolism in higher Eukaryotes. Our work also opens perspectives regarding the possible regulatory roles of the aslncRNA-derived peptides
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Yeramala, Lahari. "Caractérisation de complexes responsables de la dégradation des ARNm non-sens." Thesis, Université Grenoble Alpes (ComUE), 2017. http://www.theses.fr/2017GREAV008/document.

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Le système de contrôle appelé dégradation des ARNm non-sens (NMD) permet de détecter puis de dégrader des ARNm contenant un codon de terminaison prématuré (PTC). Les facteurs principaux de la NMD : UPF1, UPF2 et UPF3 reconnaissent les PTCs en interagissant avec les facteurs de terminaison eRF1, eRF3 et la protéine Poly(A) binding (PABP). La reconstitution d’un système de traduction in vitro a permis d’étudier la terminaison de la traduction en présence des facteurs PABP et UPF1, à l’aide de méthodes de biochimie et de cryo-microscopie électronique. L’étude du rôle du facteur de NMD UPF3B dans la terminaison de la traduction a mis en évidence une double action de cette protéine ; tout d’abord, un retardement de la reconnaissance du codon stop et également la promotion de la dissociation du ribosome. Ce travail a également permis de mettre en évidence une nouvelle interaction entre UPF3B et la kinase SMG1-8-9 et de montrer comment cette interaction affecte l’état de phosphorylation de UPF1. Les résultats de cette étude montrent une interaction complexe entre les différents facteurs de NMD et la kinase SMG1
Nonsense-mediated mRNA decay (NMD) is an important eukaryotic quality control mechanism that recognizes and degrades mRNA containing a premature termination codon (PTC). Up-frameshift proteins constitute the conserved core NMD factors (UPF1, UPF2 and UPF3). They mediate the recognition of a NMD substrate, i.e. a ribosome stalled at a PTC. UPF proteins were shown to associate with eukaryotic release factors (eRF1 and eRF3) and were suggested to impede translation termination. We showed that, at a normal termination codon, Poly(A)-binding protein (PABP) stimulates translation termination by directly interacting with eRF3a. Using a reconstituted in vitro translation system, we studied translation termination in the presence of the factors PABP and UPF1 using biochemistry and single particle electron cryo-microscopy (Cryo-EM). Additionally, we analysed the role of the other NMD factors UPF2 and UPF3B in translation termination in vitro. We discovered a novel role for UPF3B in translation termination. Moreover, we observed a novel interaction between UPF3B and the SMG1-8-9 kinase complex. The presence of UPF3B affects the kinase activity of SMG1 and thus the phosphorylation state of UPF1. Our results highlight a much more complex interplay of the NMD factors with the translation termination machinery and SMG1 kinase than anticipated
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Neusiedler, Julia. "Etude du rôle de la protéine INT6 dans la dégradation des ARN par la voie du "Nonsense Mediated mRNA Decay" (NMD) et dans la traduction et la dégradation des ARN histones." Phd thesis, Ecole normale supérieure de lyon - ENS LYON, 2011. http://tel.archives-ouvertes.fr/tel-00736233.

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Différentes observations montrent que la protéine INT6 humaine possède une activité suppresseur de tumeurs. Il a été démontré que chez l'homme le gène int6 était sous-exprimé dans environ 30% des cancers du poumon non à petits cellules et que cette sous-expression était un facteur de mauvais pronostic. Des expériences de criblage double hybride avec INT6 comme appât ont identifié une protéine nommée SLIP1 (SLBP Interacting Protein 1). Un effet de SLIP1 sur la traduction des ARN messager des histones a été montré. Les travaux que j'ai menés indiquent qu'INT6 en interagissant avec SLIP intervient dans le contrôle de la stabilité et de la traduction des ARNs codant pour les histones. Un knockdown d'INT6 provoque une baise des niveaux des histones endogènes sans avoir un effet au niveau d'ARN. Mes études, en révélant un nouveau mécanisme de dans lequel INT6 joue un rôle direct, permettent ainsi de faire le lien entre - d'une part - les fonctions connues de cette protéine dans la traduction et son contrôle et - d'autre part - les effets oncogéniques connus de son altération. Par ailleurs, l'étude de la fonction d'INT6 dans les cellules humaines réalisée par ARN interférence montre une inhibition de la dégradation des ARNm possédant un codon stop prématuré par la voie du Nonsense Mediated mRNA Decay (NMD). Nous avons étudié son action par rapport aux ARNs HTLV-1. Nous avons observé une stabilisation significative des cibles de NMD. Ceci démontre que la protéine Tax interfère avec cette voie de dégradation des ARN d'une part en empêchant l'interaction entre UPF1 et INT6 et d'autre part en interagissant lui-même avec la protéine UPF1 phosphorylée. En agissant sur le NMD, Tax intervient à un niveau post transcriptionel qui pourrait avantager la réplication virale et aussi permettre la tolérance cellulaire aux mutations liées à l'effet mutagénique établi de Tax.
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Brogna, Saverio. "Nonsense-mediated mRNA reduction and pre-mRNA processing in Drosophila." Thesis, Open University, 2000. http://oro.open.ac.uk/54807/.

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Bharudin, I. "The role of decapping factors during Nonsense-Mediated Decay (NMD) in Aspergillus nidulans." Thesis, University of Liverpool, 2016. http://livrepository.liverpool.ac.uk/3004998/.

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RNA degradation is ubiquitous and it is clear that it must be carefully controlled to accurately recognise and target appropriate transcripts. There are several pathways for mRNA degradation and decapping is one of the critical steps in determining transcript stability. The focus of this study was the identification and characterisation of factors involved in decapping and their involvement in nonsense-mediated mRNA decay (NMD) in Aspergillus nidulans. Our studies have shown that disruption of two decapping factors, Dcp1 and the Nudix protein Dcp2, lead only to partial suppression of NMD. This distinguishes A. nidulans from Saccharomyces cerevisiae, where the two decapping factors are required for NMD. Deletion of lsm1, which encodes a component of a heptomeric complex, Lsm1-7, a known promoter of decapping, also partially supressed NMD. To our knowledge this is the first time that the role of Lsm’s in NMD has been described. A similar result was observed when another Nudix family protein, NdxD, was disrupted. We propose that NdxD is a second decapping factor in A. nidulans. Disruption of other factors known to promote decapping and subsequent RNA degradation, Pat1, Dhh1 and Xrn1, did not affect NMD, demonstrating these factors are not required for NMD in A. nidulans. In order to quantify decapping, we set out to establish a simple and reliable assay to quantify the decapped transcripts. The method utilised splinted-ligation through which an RNA adaptor is ligated specifically to the 5’ end of decapped transcripts with the help of splint primer. The primer has a complementary sequences to the RNA adaptor at its 3’ end and the eight random nucleotides at the 5’ end to facilitate hybridisation to any decapped transcript. qRT-PCR was utilised to amplify the ligation products for a specific transcript and used internal primers as a control to assess the relative level of decapped transcripts. This gave a good basis for quantifying the decapped transcripts, however further optimisation is required in order to develop a robust assay. Although it has been known that both Dcp1 and Dcp2 form a decapping complex in yeast, our studies showed that Dcp2 has a significant role in stabilising the uaZ+ transcript, while deletion of dcp1 did not. Fluorescence microscopy has shown that both of these proteins localise primarily to the expected P-body like structures, however, the major proportions of Dcp2 and Dcp1 did not co-localise and were therefore not interacting. These data suggest that the Dcp2 activity is not solely dependent on Dcp1, suggesting a divergence between A. nidulans and S. cerevisiae. Additionally, confocal microscopy was used to characterise the intracellular distribution of CutA and CutB, which are involved in 3’ pyrimidine-tagging of transcripts, promoting decapping and degradation of mRNA. Using GFP and RFP tagged proteins, we determined that CutA is primarily localised in the cytoplasm whereas CutB is primarily, but not exclusively, located in the nuclei. Interestingly deletion of cutB lead to increased levels of CutA in the nuclei suggesting an interplay between the two proteins. Deletion of dcp1 produces an aberrant polysome profile as determined by sucrose gradient centrifugation. The predominant peak correlated with the large (60S) subunit rather than the monosome (80S) peak observed for WT. The small (40S) subunit was also relatively high. These observations distinguished ∆dcp1 from WT and the phenotype of the ∆dcp2 strain was intermediate between the two. The accumulation of 60S peak in ∆dcp1 included a relatively high proportion of 28S rRNA derived fragments. Northern analysis of these putative 60S degradation products and sequencing of two specific fragments suggest that in the ∆dcp1 strain the ribosomes are being cleaved, possibly as part of an rRNA turnover mechanism. Although genetic analysis showed that both ∆dcp2 and a point mutation, dcp2 E148Q, which is likely to disrupt the nuclease activity, are both epistatic to dcp1 with respect to this phenotype. Northern analysis indicates that the degradation products observed in ∆dcp1, ∆dcp2 and WT strains appear very similar, even though the levels vary dramatically. This implies that Dcp2 is probably not directly responsible for these cleavage events or it is one of a number of activities cleaving the rRNA in what appears to be a similar way.
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Chicois, Clara. "Study of the interactome of UPF1, a key factor of Nonsense-mediated decay in Arabidopsis thaliana." Thesis, Strasbourg, 2018. http://www.theses.fr/2018STRAJ005.

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L’ARN hélicase UPF1 est un facteur clé du Nonsense-Mediated Decay (NMD), un mécanisme impliqué dans le contrôle de la qualité des ARNm et la régulation de l’expression des gènes. Malgré d’importantes fonctions chez les plantes, le NMD y est peu décrit. Cette thèse présente l’identification et l’étude des protéines interagissant avec UPF1 chez Arabidopsis. Nous avons identifié un nouveau réseau d’interaction protéine-protéine entre UPF1 et des répresseurs de traduction dans les P-bodies. Nous proposons un modèle dans lequel la répression traductionnelle exerce une action protectrice sur les cibles du NMD. Notre approche a également identifié de nouveaux composants des P-bodies, comme l’endonucléase UCN. Son étude détaillée a révélé un lien direct avec la machinerie de decapping ainsi que de possibles rôles dans la signalisation hormonale ou les mécanismes de défense, suggérant que la modulation de l’expression d’UCN pourrait influencer d’importantes caractéristiques agronomiques. Ce travail décrit des facteurs associés à UPF1 jusqu’alors inconnus, leur étude permettra de découvrir de nouveaux mécanismes impliqués dans l’équilibre entre la traduction, le stockage et la dégradation des ARNm chez les plantes
The RNA helicase UPF1 is a key factor of Nonsense-Mediated Decay (NMD), a paneukaryotic mechanism involved in mRNA quality control and fine-tuning of gene expression. Despite important biological functions in plants, NMD is poorly described compared to other eukaryotes. This thesis presents the identification and study of UPF1 interacting proteins in Arabidopsis. Using approaches based on immunoaffinity and mass spectrometry, we identified a novel protein-protein interaction network between UPF1 and translation repressors in P-bodies. We propose a model in which translation repression exerts a protective action on NMD targets in plants. Our approach also identified novel P-body components, including the UCN endonuclease. A detailed study revealed its direct link with the decapping machinery and possible roles in hormone signaling and defense mechanisms, suggesting that the modulation of UCN expression could influence important agronomical traits. This work describes hitherto unknown UPF1 associated factors, their study will provide novel insights into the mechanisms involved in the balance between mRNA translation, storage and decay in plants
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8

Bokhari, A'Dem. "Etude de la mutation de la chaperonne HSP110 dans les cancers gastro-intestinaux MSI : conséquences fonctionnelles et cliniques." Thesis, Paris 6, 2017. http://www.theses.fr/2017PA066239/document.

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L'instabilité microsatellitaire (MSI) résulte d'une déficience du système de réparation des mésappariements de l'ADN. Cette instabilité est observée dans 10-15% des tumeurs chez l'Homme, incluant les cancers colorectaux (CCR) et de l'estomac (CG). En 2011, notre laboratoire a rapporté la mutation de la chaperonne HSP110 dans les CCR MSI. Cette mutation affecte un microsatellite intronique de 17 thymidines (T17), localisé au niveau de l'intron 8. Les grandes délétions somatiques du T17 (? 5 paires de bases), représentant 25% des CCR MSI, conduisent à l'inactivation complète de la chaperonne HSP110 dans les CCR MSI. De manière remarquable, ces grandes délétions sont prédictives chez les patients d'une excellente réponse à la chimiothérapie adjuvante. Au cours de ma thèse, mes travaux ont visé à étudier l'impact de la mutation d'HSP110 dans les tumeurs gastro-intestinales MSI. Mes résultats démontrent que la mutation du microsatellite T17 d'HSP110 a pour conséquence une diminution de la prolifération cellulaire en partie lié à la diminution de la phosphorylation du facteur de transcription STAT3. En outre, mes résultats suggèrent que cette mutation serait un facteur prédictif de survie chez les patients atteint de CG, indiquant le potentiel théranostique d'HSP110. Enfin, je propose une approche thérapeutique innovante pour les patients atteints de CCR MSI, basée sur la potentialisation de l'expression de transcrits mutants, codant pour des protéines délétères pour la cellule tumorale, à l'instar du dominant négatif HSP110DE9 résultant de la mutation d'HSP110 dont l'ARN semble être régulé par le système NMD (Nonsense-Mediated mRNA Decay)
Microsatellite instability (MSI) results from impaired DNA mismatch repair, being observed in 10-15% of frequent tumors in human, e.g. Colorectal (CRC), Gastric Cancers (GC) and others. In 2011, frequent somatic mutations of the HSP110 chaperone have been reported in MSI CRC by my lab, affecting a T17 intronic DNA repeat located in intron 8. Large (≥ 5 base pairs) bi-allelic somatic deletions of this DNA repeat in tumor DNAs, as observed in about 25% of MSI CRC, lead to complete inactivation of HSP110 by exon 9 skipping and sensitization of tumor cells to chemotherapy. These large deletions are predictive of improved response to adjuvant chemotherapy in CRC patients. During my PhD thesis, I further investigated the role of HSP110 in MSI tumors. My results demonstrate that HSP110 mutation leads to cell proliferation decrease through the reduction of STAT3 transcription factor phosphorylation in CRC tumors (Berthenet*, Bokhari*, et al., Oncogene 2016). Furthermore, I showed that HSP110 mutation is also frequently observed in MSI gastric cancer, leading to very similar pathophysiological consequences during tumor progression and improved patient’s survival independently from tumor stage (Cervera*, Lagrange*, Bokhari* et al., submitted). Finally, I worked on an innovative therapeutic approach that consisted in inhibiting the NMD (Nonsense-Mediated mRNA Decay) system, an ubiquitous process recognizing and degrading mRNAs containing premature termination codons (PTC). The inhibition of NMD leads to the expression of deleterious MSI-driven mutant transcripts such as the HSP110DE9, coding for a dominant negative mutant, derived from HSP110 mutation in MSI cancer cells
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9

Gilbert, Agathe. "Impact of protein-protein interactions and phosphorylation on RNA decapping for nonsense mediated mRNA decay (NMD)." Electronic Thesis or Diss., Sorbonne université, 2022. http://www.theses.fr/2022SORUS386.

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Chez Saccharomyces cerevisiae, la voie de dégradation majoritaire des ARN messagers passe par le clivage de la liaison pyrophosphate entre l’ARNm et la structure de la coiffe à l’extrémité 5’. Cette étape, importante pour la dégradation de l’ensemble des ARNm, est particulièrement clé dans la dégradation d’une classe d’ARN instables, cibles de la voie de dégradation nommée nonsense-mediated mRNA decay (NMD). Cette-dernière permet la dégradation de transcrits contenant un codon STOP prémature et donc dépend de la traduction. D’abord considérée comme une voie de dégradation présente à travers les eucaryotes à cause de la grande conservation de ses facteurs principaux – les protéines Upf -, la découverte des protéines Smg dans C. elegans (Page et al., 1999) et la description du mécanisme SURF/DECID dépendant de la phosphorylation d’Upf1 (Kashima et al., 2006) semblaient indiquer des différences majeures entre les organismes. Récemment, notre laboratoire a décrit l’architecture des complexes NMD chez la levure. Ces-derniers sont centrés autour d’Upf1 et ont été nommés Détecteur et Effecteur. Dans le second, nous avons pu identifier la protéine kinase Hrr25 comme un membre du complexe Upf1 avec les protéines du decapping, Dcp2, Dcp1 et Edc3 (Dehecq et al., 2018). Cette protéine conservée est l’analogue des caséines kinases 1 chez l’humain - CK1delta and CK1epsilon - et elle est impliquée dans de nombreux processus majeurs de la cellule, comme la modification des ARNt, la biogénèse des ribosomes, l’élongation de la transcription et la méiose (Abdel-Fattah et al., 2015 ; Ghalei et al., 2015 ; Ye et al., 2016 ; Nemec et al., 2019). J’ai montré que l’activité kinase de Hrr25 a un rôle dans le NMD qui est indépendant de ses fonctions dans la traduction de l’ARNm mais aussi dans la transcription de l’ADN. Nous avons aussi montré que l’association de Hrr25 avec Upf1 s’appuie sur l’activité kinase de Hrr25 et sur la présence de la protéine portant l’activité decapping, Dcp2. Nous avons pu identifier des résidus Sérine très conservées dans la région C-terminal d’Upf1 levure dont la phosphorylation dépend de Hrr25 et dont la régulation, à l’image de celle impliquée dans d’autres organismes, dépend de la présence d’autres facteurs NMD comme Upf2 et Ebs1 (l’équivalent de Smg5/7). Ces résultats indiquent que les protéines kinase peuvent moduler le NMD par des interactions directes avec les enzymes impliquées dans la dégradation des ARN. Ils suggèrent également que, contrairement à ce que l’on pouvait croire, des protéines kinase sont requises de manière universelle pour le NMD
In yeast, mRNA degradation is mainly initiated through the cleavage of the pyrophosphate bond between the mRNA and the cap structure at its 5’-end. While this step is important for the decay of most mRNAs, it is particularly critical to initiate the degradation of unstable RNA, targets of the NMD machinery. This pathway allows degradation of transcripts that contain a premature termination codon and thus is entirely dependent on translation. First considered as conserved throughout eucaryotes due to high sequence similarity of its core factors – the Upf proteins -, the discovery of the Smg proteins in C. elegans (Page et al., 1999) and the description of the SURF/DECID mechanism depending on phosphorylation of Upf1 (Kashima et al., 2006) indicated a divergence of NMD mechanisms between organisms. However, recently our laboratory described two NMD complexes revolving around Upf1 – named Detector and Effector - and identified the protein kinase Hrr25 as a member of a Upf1-decapping complex (Dehecq et al., 2018). The conserved protein kinase Hrr25 is the yeast equivalent of mammalian casein kinase 1 (CK1delta and CK1epsilon) and is involved in major cellular processes, including tRNA modification, ribosome biogenesis, transcription elongation and meiosis (Abdel-Fattah et al., 2015; Ghalei et al., 2015; Ye et al., 2016; Nemec et al., 2019). I demonstrated that the Hrr25 kinase activity has a role in NMD that is independent of its function in mRNA translation and DNA transcription. The association of Hrr25 to Upf1 was dependent on the kinase activity of the protein and on the presence of the decapping enzyme Dcp2. We identified conserved serine residues located in the C-terminal region of yeast Upf1 whose phosphorylation was dependent on Hrr25 and was modulated, like the phosphorylation of Upf1 in other organisms, by the presence of other NMD factors, such as Upf2 and Ebs1 (SMG5/7 equivalent). These results indicate that protein kinases can modulate NMD by direct interactions with the enzymes involved in RNA degradation and suggest that, contrary to previous beliefs, protein kinases are universally required for NMD
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Durand, Sébastien. "Développement de molécules chimiques capables d’inhiber l’épissage et le Nonsense-Mediated mRNA Decay (NMD)." Montpellier 2, 2008. http://www.theses.fr/2008MON20072.

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L'épissage des pré-ARNm, le processus nucléaire conduisant à l'assemblage des séquences "exons" de l'ARN messager par élimination des séquences intercalaires ou "introns", est une étape décisive de l'expression de la plupart des gènes chez les métazoaires. Au cours de ce processus, beaucoup d'erreurs peuvent survenir avec des conséquences plus ou moins graves pour le bon fonctionnement de la cellule. Afin de limiter les effets délétères de telles erreurs, différents mécanismes de contrôle de qualité des ARNm épissés ont été mis en place. Parmi eux, le Nonsense-Mediated mRNA Decay (NMD) permet de dégrader les ARNm contenant des codons non-sens prématurés (PTC), évitant ainsi l'apparition de protéines tronquées. De par leur ampleur en tant que mécanismes centraux de l'expression génique chez l'homme, l'épissage et le NMD sont fréquemment impliqués dans des pathologies d'origine génétique. Dans certains cas comme l'ataxie télangiectasie ou la neurofibromatose de type I, 54% des mutations responsables de la maladie affectent l'épissage. Environ un tiers des maladies génétiques sont dues à l'apparition de PTC qui induisent le NMD. Dans certains cas, une protéine tronquée pourrait conserver les mêmes propriétés que la protéine sauvage mais le mécanisme de NMD empêche sa synthèse. Par conséquent, l'épissage et le NMD représentent des cibles tout à fait intéressantes qui permettraient, soit de restaurer un épissage correct, soit de permettre l'expression de protéines tronquées et fonctionnelles. Au cours de cette thèse nous avons recherché des inhibiteurs d'épissage et/ou de NMD parmi une collection de 6 000 composés chimiques. Nous avons ainsi pu identifier des composés capables de moduler l'épissage en affectant l'activité de facteurs clefs de la sélection des sites d'épissage, les protéines SR. Nous avons également mis en évidence le premier inhibiteur spécifique du NMD qui bloque spécifiquement la fonction du facteur hUpf1. Ces molécules nous ont permis de disséquer le fonctionnement de ces processus, de proposer un nouveau modèle décrivant le transit des mRNP soumises au NMD par les P-Bodies et ouvrent maintenant la voie à la mise en place de nouvelles stratégies thérapeutiques utilisant ces composés
RNA splicing involves the processing of pre-messenger RNA molecules by the excision of introns and the precise joining of exons to form the mature messenger RNA that is exported from the nucleus for translation. Exon usage is often alternative, i. E. The cell decides whether to remove a part of the pre-mRNA as an intron or include this part in the mature mRNA as an alternative exon. Alternative splicing is therefore, a genetically economical process that enables a single gene to increase its coding capacity, allowing the synthesis of several structurally and functionally distinct protein isoforms. To avoid accumulation of aberrantly spliced mRNAs, several quality control processes determine the fate of mRNA in the cell. Among these processes, Nonsense-Mediated mRNA decay (NMD), is able to degrade mRNA containing premature termination codons (PTCs), preventing accumulation of truncated with deleterious effects for the cell. As central mechanisms controlling gene expression any disturbance of either splicing or NMD can lead to genetic diseases. Indeed, the numbers of diseases shown to be caused by a defect in pre-mRNA splicing or NMD is rapidly growing. For example, in ataxia telengectasia or type I neurofibromatosis, 54% of disease-inducing mutations affect mRNA splicing. Moreover, one third of acquired and inherited pathologies are due to nonsense creation that elicits NMD. Consequently, mRNA splicing and NMD represent a potential targets for new therapeutic strategies. During this thesis, we have screened a small chemical library to find splicing and NMD inhibitors. We have identified some molecules that modulate mRNA splicing efficiency by affecting SR proteins activity. We have also isolated the first specific inhibitor of NMD that blocks hUpf1 functions. These compounds allowed us to decipher splicing and NMD mechanisms and to propose a new model to describe the NMD-subjected mRNP transit trough the processing-Bodies. The next challenge will be to demonstrate the functional utility of these molecules in preclinical models of human disease
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Books on the topic "NMD"

1

NMD yu fan zhi NMD. Beijing: Guo fang da xue chu ban she, 2001.

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Homan, C. NMD: De Amerikaanse waterlinie. 's-Gravenhage: Nederlands Instituut voor Internationale Betrekkingen Clingendael, 2000.

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Centre for Indian Political Research & Analysis., ed. NMD in South Asia. Delhi: Centre for Indian Political Research and Analysis, 2001.

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Nord, Archives départementales du, ed. Bazuel: BMS et NMD, 1764-1882. Valenciennes: Association généalogique Flandre Hainaut, 2003.

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Lawniczak, Catherine. Amfroipret: NMD de 1843 à 1905. Berlaimont: Cercle historique et généalogique de Berlaimont, 2008.

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Lawniczak, Catherine. Amfroipret: NMD de 1843 à 1905. Berlaimont: Cercle historique et généalogique de Berlaimont, 2008.

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Moreau, Claude. Bazuel: BMS et NMD, 1764-1882. Valenciennes: Association généalogique Flandre Hainaut, 2003.

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Lawniczak, Catherine. Amfroipret: NMD de 1843 à 1905. Berlaimont: Cercle historique et généalogique de Berlaimont, 2008.

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Chŏn, Sŏng-hun. Miguk ŭi NMD kuchʻuk kwa Hanbando ŭi anjŏn pojang. Sŏul Tʻŭkpyŏlsi: Tʻongil Yŏnʾguwŏn, 2001.

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Balligand, Laurent. Eclaibes: NMD de 1802 à 1904 : parcellaire de 1694 à 1802. Berlaimont: Cercle historique et généalogique de Berlaimont, 2007.

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Book chapters on the topic "NMD"

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Eckersall, Peter, Helena Grehan, and Edward Scheer. "Post-NMD?" In New Media Dramaturgy, 209–12. London: Palgrave Macmillan UK, 2017. http://dx.doi.org/10.1057/978-1-137-55604-2_9.

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Iatsenko, Dmytro. "Nonlinear Mode Decomposition (NMD)." In Springer Theses, 59–81. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-20016-3_4.

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Hafemeister, David. "The Defense: ABM/SDI/BMD/NMD." In Physics of Societal Issues, 77–105. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-9272-6_3.

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Sejerson, Thomas, and Kate Bushby. "Standards of Care for Duchenne Muscular Dystrophy: Brief Treat-NMD Recommendations." In Advances in Experimental Medicine and Biology, 13–21. Dordrecht: Springer Netherlands, 2009. http://dx.doi.org/10.1007/978-90-481-2813-6_2.

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Lei, Tingyu, Xingchen Liu, and Xiaodong Wen. "Chapter 7. Modeling Nanocatalytic Reactions with DFTB/MM-MD and DFTB-NMD." In Theoretical and Computational Chemistry Series, 203–26. Cambridge: Royal Society of Chemistry, 2021. http://dx.doi.org/10.1039/9781839164668-00203.

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Kurosaki, Tatsuaki, Mainul Hoque, and Lynne E. Maquat. "Identifying Cellular Nonsense-Mediated mRNA Decay (NMD) Targets: Immunoprecipitation of Phosphorylated UPF1 Followed by RNA Sequencing (p-UPF1 RIP−Seq)." In mRNA Decay, 175–86. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7540-2_13.

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Kimmich, Rainer. "Introductory Remarks." In NMR, 3–6. Berlin, Heidelberg: Springer Berlin Heidelberg, 1997. http://dx.doi.org/10.1007/978-3-642-60582-6_1.

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Kimmich, Rainer. "Spin-Relaxation Functions." In NMR, 90–96. Berlin, Heidelberg: Springer Berlin Heidelberg, 1997. http://dx.doi.org/10.1007/978-3-642-60582-6_10.

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Bormann, Natalie. "NMD." In National missile defence and the politics of US identity. Manchester University Press, 2013. http://dx.doi.org/10.7765/9781847792075.00007.

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Neu‐Yilik, Gabriele, and Andreas E. Kulozik. "Chapter 4 NMD." In Advances in Genetics, 185–243. Elsevier, 2008. http://dx.doi.org/10.1016/s0065-2660(08)00604-4.

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Conference papers on the topic "NMD"

1

Almeida, Ana Elizabeth Cunha Guimarães de, William Nicoleti Turazza da Silva, Maria Fernanda Prado Rosa, Isabella Cristina Guimarães de Almeida, Ana Clara Gondim Oliveira, Beatriz Iolanda de Sene Ferregutti Pinheiro, Elisa Santos Pennisi, et al. "Early non-invasive ventilation indication in amyotrophic lateral sclerosis and other neuromuscular disorders: a prospective study." In XIV Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2023. http://dx.doi.org/10.5327/1516-3180.141s1.759.

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Introduction: Neuromuscular diseases (NMD) affect the peripheral nervous system and may lead to progressive respiratory failure. Ventilatory assistance reduces dyspnea and improves quality of life. Objectives: The aim of this study is to compare patients with amyotrophic lateral sclerosis (ALS) or other NMD and the effects of early indication of noninvasive ventilation (NIV) (FVC > 70). Methods: A study was carried out in patients with NMD and indication for NIV, accompanied by periodic examinations, weekly telemonitoring and adjustments of ventilatory parameters for six months. Results: The study found that ALS patients had greater adherence to NIV, with mean daily use increasing from 4.7 to 6.0 hours and a decrease in leakage (L/min) from 2.5 to 1.5 and in the apnea-hypopnea index (AHI) from 5.85 to 4.85. Patients with other NMDs had a decrease in mean daily use from 6.1 to 5.3 hours, with a decrease in leakage from 1.2 to 0.5 and AHI from 3.1 to 1.9. Patients with early indication for NIV had a lower rate of deaths and noncompliance compared to those with late indication. Patients with early indication had 6 hours (±2.0) of average daily use and maintained it after 6 months (±1.3) with a decrease in leakage from 1.9 to 0.2 and AHI from 3.1 to 2, two. In the late indication group, there were 4 deaths and 2 dropouts, with an increase in daily use from 4.7 to 5.5 hours, a decrease in leakage from 1.9 to 1.5 and AHI from 3.2 to 2.2. Conclusion: This study suggests that early NIV indication can improve ventilatory parameters and outcomes in patients with NMDs, especially ALS, and should be considered for patients with FVC > 70%.
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Lopes, Carla, and Fernando Perdigao. "Speech event detection using SVM and NMD." In 2007 9th International Symposium on Signal Processing and Its Applications (ISSPA). IEEE, 2007. http://dx.doi.org/10.1109/isspa.2007.4555570.

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Cody, V., and V. Grimes. "National Missile Defense (NMD) System Integration Test." In Space Programs and Technologies Conference and Exhibit. Reston, Virigina: American Institute of Aeronautics and Astronautics, 1993. http://dx.doi.org/10.2514/6.1993-4071.

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Okkenhaug, Siril, Bjo̸rn Sogstad, and Jan Mathisen. "Applying Partial Safety Factors in Mooring System Design." In ASME 2005 24th International Conference on Offshore Mechanics and Arctic Engineering. ASMEDC, 2005. http://dx.doi.org/10.1115/omae2005-67111.

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The DNV offshore standard for position mooring, DNV-OS-E301 [1], was issued June 2001 based on the result from a joint industry project. A new revision was issued in October 2004. The consequences for mobile units when applying the new standard, compared to the old class rules, have been a major concern for operators of mobile units. A comparison study has therefore been initiated, where four relevant units are considered. We have applied the mooring design for existing mobile units that operate in Norwegian waters. Two different water depths are covered. The new standard, DNV-OS-E301, applies a partial safety factor format. However, the main difference when applying DNV-OS-E301 compared to the old POSMOOR [2] rules is that low frequency (LF) motions will have to be taken into account when calculating the line tensions. The results for the four mobile units are compared also to other relevant codes, i.e. the Draft International Standard ISO 19901-7 [4] and the present Norwegian regulations for offshore structures, NMD [5 & 6]. It should be noted that the present NMD regulations still do not require that LF motions are taken into account. Due to the partial safety factor format in DNV-OS-E301, more or less all of the units fulfill the requirements even though LF motion is accounted for. However, when comparing the results to the NMD regulations, the introduction of LF motion is crucial for almost all of the mobile units studied, as they have problems in fulfilling the requirements when this response is accounted for. Simply including LF motion in design would tend to increase the required strength of the resulting mooring line designs, and thereby raise the safety level if nothing else is done with the NMD regulations. Thus, provided that the present safety level for mobile units is sound, the present NMD safety factors could either be reduced or the partial factor format in DNV-OS-E301 could be adopted in order to maintain the safety level for mobile units when LF motion is taken into account.
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Sunkara, Nageswara, and Sankar Dayal Theenadhayalan. "Conceptual Design of Dahej-Nagothane Ethane Pipeline in India." In ASME 2019 India Oil and Gas Pipeline Conference. American Society of Mechanical Engineers, 2019. http://dx.doi.org/10.1115/iogpc2019-4512.

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Reliance Industries Limited (RIL) planned to import liquid Ethane from North American market for use as feedstock in Gas Crackers at Dahej Manufacturing Division (DMD), Hazira Manufacturing Division (HMD) in the state of Gujarat and Nagothane Manufacturing Division (NMD) in the state of Maharashtra. Liquid Ethane was planned to be unloaded at GCPTCL (Gujarat Chemical Port Terminal Company Limited) Jetty and stored in cryogenic tank in DMD. For use in NMD and HMD, it was proposed to transport Ethane via a dedicated pipeline traversing through the states of Gujarat and Maharashtra and deliver at respective gas crackers of HMD and NMD in a direct usage mode as no storage facilities for Ethane were envisaged at delivery locations. Reliance Gas Pipelines Limited (RGPL), a wholly owned subsidiary of RIL implemented the Asia’s 1st liquid Ethane Pipeline project as “Dahej - Nagothane Ethane Pipeline Project” (DNEPL) and successfully commissioned the pipeline in September, 2018. This paper presents the Conceptual Design of the project including selection of phase of transportation, pipeline configuration in terms of pipeline size, no. of pump stations, spacing of main line valves (MLV’s), operating conditions, material of construction and emergency evacuation requirements of Ethane during long haul transportation.
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Shaul, Orit. "The NMD factor UPF3 is essential for plant salt tolerance." In ASPB PLANT BIOLOGY 2020. USA: ASPB, 2020. http://dx.doi.org/10.46678/pb.20.149030.

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Jannson, Tomasz P., Andrew A. Kostrzewski, and Igor V. Ternovskiy. "Superfast supercomputer-class on-board processing for visual sensor NMD applications." In Aerospace/Defense Sensing, Simulation, and Controls, edited by Alex F. Sisti and Dawn A. Trevisani. SPIE, 2001. http://dx.doi.org/10.1117/12.440058.

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Almeida, Ana Elizabeth Cunha Guimarães de, William Nicoleti Turazza da Silva, Isabella Cristina Guimarães de Almeida, Iago Resende Carvalho, João Augusto Nunes Vitorino, Beatriz Iolanda de Sene Ferregutti Pinheiro, Elisa Santos Pennisi, et al. "Ventilatory support and telemonitoring in patients with neuromuscular disease: a prospective study." In XIV Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2023. http://dx.doi.org/10.5327/1516-3180.141s1.720.

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Introduction: Neuromuscular disorders (NMD) are diseases of the peripheral nervous system with systemic manifestations. The ventilatory impairment could be one of the most serious complications and can lead to respiratory failure, either chronically or acutely. Objectives: To describe the effects of non-invasive ventilation (NIV) associated with telemonitoring in patients with NMD. Methods: A prospective study of patients with NMD and indication for NIV due to a reduced FVC on spirometry or respiratory symptoms was done. These patients were followed up with periodic exams, telemonitoring and adjustments of ventilatory parameters for six months. Results: 37 patients were included, 56.7% male, average age 49.7 years (±12.6). 69.5% reported dyspnea before the indication of NIV and 10% needed medical attention. The average forced vital capacity (FVC) at inclusion was 67.7 (±14.9) and 72.4 (±15.7) after six months, with average diurnal oxygen arterial saturation of 95.22 (±5.4) at inclusion and 95.7 (±5.1) after 6 months. Throughout the study, 4 (10.8%) patients died and 2 (5.4%) underwent tracheostomy. Between inclusion and after 6 months, according to telemonitoring, there was an increase in the average daily use in hours from 5.5 (±2.2) to 5.6 (±2.0), with a drop in leakage (L/min) from 1.9 (±6. 6) to 1.0 (±7.0) and in the AHI from 3.15 (±4.9) to 2.2 (±4.3). Conclusion: Diurnal oxygen arterial saturation was not a good parameter for indicating NIV, as well as FVC < 70, since most patients already had respiratory manifestation. Regular follow-up of patients associated with telemonitoring showed an improvement in ventilatory parameters, maintaining stability in adherence to therapy over the six months.
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Dwarakanath, Akshay, Sanjay Bangad, Joseph Hogg, Husham Elfaki, Mohammed Khan, Anjali Gondker, Muthu Thirumaran, Salim Meghjee, and Anthony Johnson. "Gastrostomy outcome in patients with Progressive Respiratory Failure (PRF) secondary to Neuromuscular Disorders (NMD)." In ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.1958.

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Rad, Arash, Marta Kaminska, Basil J. Petrof, Larry C. Lands, Zoltan Hantos, Ronald J. Dandurand, and Stewart B. Gottfried. "Oscillometry (OSC) to assess respiratory function in rare neuromuscular disease with respiratory muscle weakness (NMD)." In ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.1905.

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Reports on the topic "NMD"

1

Swenson, Robert. NMD BM/C3 Implementation,. Fort Belvoir, VA: Defense Technical Information Center, September 1996. http://dx.doi.org/10.21236/ada319963.

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Manuel, Henry, Jack Sliney, John Cummings, and Dave Grover. Ensuring NMD Affordability Through the PSAoRm Process,. Fort Belvoir, VA: Defense Technical Information Center, January 1997. http://dx.doi.org/10.21236/ada328982.

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Bertucchi, Marc R. U.S. National Missile Defense (NMD) and European Security. Fort Belvoir, VA: Defense Technical Information Center, March 2001. http://dx.doi.org/10.21236/ada394218.

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Barrett, David K. National Missile Defense (NMD) -- Has Its Time Come? Fort Belvoir, VA: Defense Technical Information Center, January 1997. http://dx.doi.org/10.21236/ada326401.

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Dobie, D. W. ACRV instrumentation plan for NMD HTK light gas gun tests. Office of Scientific and Technical Information (OSTI), April 1999. http://dx.doi.org/10.2172/10790.

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Gerassimenko, M. LLNL Modeling Calculations in Support of the NMD EOS Program: FY01 3Q Report (U). Office of Scientific and Technical Information (OSTI), July 2001. http://dx.doi.org/10.2172/15007274.

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Ionov, Yurij. Identification of Prostate Cancer-Related Genes Using Inhibition of NMD in Prostate Cancer Cell Lines. Fort Belvoir, VA: Defense Technical Information Center, January 2005. http://dx.doi.org/10.21236/ada435274.

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Ionov, Yurij. Identification of Prostate Cancer-Related Genes Using Inhibition of NMD in Prostate Cancer Cell Lines. Fort Belvoir, VA: Defense Technical Information Center, January 2007. http://dx.doi.org/10.21236/ada465202.

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Ionov, Yurij. Identification of Prostate Cancer Related Genes Using Inhibition of NMD in Prostate Cancer Cell Lines. Addendum. Fort Belvoir, VA: Defense Technical Information Center, January 2008. http://dx.doi.org/10.21236/ada479284.

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van den Oever, Martien, Iris Vural Gursel, Helmer Weterings, Eric de Munck, Fred van der Burgh, Sissy Verspeek, and John Drissen. Bio-based building products in the Dutch Environmental Database (NMD). Part 1, Proposal for crediting biogenic carbon storage. Wageningen: Wageningen Food & Biobased Research, 2024. http://dx.doi.org/10.18174/647711.

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